Journal articles on the topic 'Eosinophic parasite'
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1
Bates, Alan W. H. "Diagnosing Eosinophilic Colitis: Histopathological Pattern or Nosological Entity?" Scientifica 2012 (2012): 1–9. http://dx.doi.org/10.6064/2012/682576.
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Reports of “eosinophilic colitis”—raised colonic mucosal eosinophil density in patients with lower gastrointestinal symptoms—have increased markedly over the last fifteen years, though it remains a rarity. There is no consensus over its diagnosis and management, and uncertainty is compounded by the use of the same term to describe an idiopathic increase in colonic eosinophils and an eosinophilic inflammatory reaction to known aetiological agents such as parasites or drugs. In patients with histologically proven colonic eosinophilia, it is important to seek out underlying causes and careful clinicopathological correlation is advised. Because of the variability of eosinophil density in the normal colon, it is recommended that histological reports of colonic eosinophilia include a quantitative morphometric assessment of eosinophil density, preferably across several sites. Few reported cases of “eosinophilic colitis” meet these criteria. As no correlation has been shown between colonic eosinophil density and symptoms in older children or adults, it is suggested that treatment should be directed towards alleviation of symptoms and response to treatment assessed clinically rather than by histological estimates of intramucosal eosinophils.
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Sturm, Eva Maria, Eva Knuplez, and Gunther Marsche. "Role of Short Chain Fatty Acids and Apolipoproteins in the Regulation of Eosinophilia-Associated Diseases." International Journal of Molecular Sciences 22, no. 9 (April 22, 2021): 4377. http://dx.doi.org/10.3390/ijms22094377.
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Eosinophils are key components of our host defense and potent effectors in allergic and inflammatory diseases. Once recruited to the inflammatory site, eosinophils release their cytotoxic granule proteins as well as cytokines and lipid mediators, contributing to parasite clearance but also to exacerbation of inflammation and tissue damage. However, eosinophils have recently been shown to play an important homeostatic role in different tissues under steady state. Despite the tremendous progress in the treatment of eosinophilic disorders with the implementation of biologics, there is an unmet need for novel therapies that specifically target the cytotoxic effector functions of eosinophils without completely depleting this multifunctional immune cell type. Recent studies have uncovered several endogenous molecules that decrease eosinophil migration and activation. These include short chain fatty acids (SCFAs) such as butyrate, which are produced in large quantities in the gastrointestinal tract by commensal bacteria and enter the systemic circulation. In addition, high-density lipoprotein-associated anti-inflammatory apolipoproteins have recently been shown to attenuate eosinophil migration and activation. Here, we focus on the anti-pathogenic properties of SCFAs and apolipoproteins on eosinophil effector function and provide insights into the potential use of SCFAs and apolipoproteins (and their mimetics) as effective agents to combat eosinophilic inflammation.
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Folkard, S. G., P. J. Hogarth, M. J. Taylor, and A. E. Bianco. "Eosinophils are the major effector cells of immunity to microfilariae in a mouse model of onchocerciasis." Parasitology 112, no. 3 (March 1996): 323–29. http://dx.doi.org/10.1017/s0031182000065847.
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SUMMARYMice inoculated with microfilariae of the filarial nematode Onchocerca lienalis clear their parasites over a period of 3–4 months and are highly resistant to re-infection. We have investigated the comparative roles of the eosinophil, macrophage and neutrophil in effecting this parasite clearance, employing agents specifically to perturb cell function in vivo. Using the anti-IL-5 monoclonal antibody TRFK-5, we show that eosinophils are of primary importance in effecting resistance to re-infection. Ablation of macrophages (with carbon) and neutrophils (with the monoclonal antibody NIMP-R14) had no effect on parasite clearance following re-infection. Neutralization of these 3 cell types during a primary infection showed that while the removal of both eosinophils and macrophages caused a small but significant delay in parasite clearance, the depletion of neutrophils had no effect. This report describes the first direct evidence for eosinophil-mediated killing of microfilariae in vivo, and is consistent with Th-2 cell responses previously described in this model.
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Kierszenbaum, F., F. Villalta, and P. C. Tai. "Role of inflammatory cells in Chagas' disease. III. Kinetics of human eosinophil activation upon interaction with parasites (Trypanosoma cruzi)." Journal of Immunology 136, no. 2 (January 15, 1986): 662–66. http://dx.doi.org/10.4049/jimmunol.136.2.662.
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Abstract The kinetics of human eosinophil activation and granule secretion initiated by interaction with Trypanosoma cruzi amastigotes was studied by using a monoclonal IgG1 antibody (termed EG2) that is specific for an epitope present only in the secreted forms of both eosinophil cationic protein (ECP) and the eosinophil protein X (EP-X), and hence not detectable in unstimulated resting eosinophils. Studies were carried out by using electron microscopy and indirect immunofluorescence. In the electron microscopy studies, deposits of protein A-gold particles in parasite-containing eosinophils that had been incubated previously with EG2 antibody were first detected 4 hr after initiation of the eosinophil-amastigote interaction. Control tests performed with a monoclonal IgG1 unreactive with eosinophils showed no deposition of protein A-gold particles. EG2 antibody binding was confined to the crystalloid granule matrix, where ECP and EP-X are known to be stored. A similar kinetic pattern of ECP/EP-X solubilization and secretion was confirmed by the results of the indirect immunofluorescence experiments also showing the binding of EG2 antibody after 4 hr of cell-parasite interaction. The kinetics of ECP/EP-X solubilization and secretion paralleled the kinetics of destruction of internalized amastigotes, suggesting a role for these basic proteins in parasite killing. Consistent with this notion was the detection of ECP/EP-X in the fluid of phagocytic vacuoles containing amastigotes and associated with the ingested organisms at the same time as the parasites began to show structural alterations. These results outlined the kinetics of eosinophil activation in terms of the time required for mobilization of two basic proteins associated with eosinophil secretion that are known to be biologically active.
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Yamaguchi, Y., Y. Hayashi, Y. Sugama, Y. Miura, T. Kasahara, S. Kitamura, M. Torisu, S. Mita, A. Tominaga, and K. Takatsu. "Highly purified murine interleukin 5 (IL-5) stimulates eosinophil function and prolongs in vitro survival. IL-5 as an eosinophil chemotactic factor." Journal of Experimental Medicine 167, no. 5 (May 1, 1988): 1737–42. http://dx.doi.org/10.1084/jem.167.5.1737.
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The recent molecular cloning of the complementary DNA encoding T cell--replacing factor (TRF) has demonstrated that a single molecule is responsible for B cell growth factor II (BCGF-II) activity and eosinophil differentiation activity. It has been proposed that this molecule be called interleukin 5 (IL-5). We previously reported that purified rIL-5 supports the terminal differentiation and proliferation of eosinophilic precursors. In this study, we examined the effects of IL-5 on functional activities of mature eosinophils. IL-5 maintained the viability of mature eosinophils obtained from peritoneal exudate cells of mice infected with parasites. It also induced superoxide anion production in a dose-dependent manner. The Boyden's chamber Millipore assay revealed that IL-5 had a marked chemokinetic effect on eosinophils in a dose-dependent manner. Moreover, IL-5 was found to be an eosinophil chemotactic factor by the checkerboard assay. In conclusion, IL-5 is suggested to play an important role in increasing the functional activities of eosinophils as well as their production in allergic and parasitic diseases.
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Macapagal, Daphne, Jane Connor, Tomas Mikael Mustelin, Thirumalai Ramalingam, Thomas Wynn, and Todd Davidson. "Necrotic liver induces pyroptosis through caspase-1 in eosinophils." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 221.8. http://dx.doi.org/10.4049/jimmunol.198.supp.221.8.
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Abstract During sterile inflammatory reactions, damage associated molecular patterns (DAMPS) are released from necrotic cells and recruit immune cells to the sites of tissue injury. We found that necrotic liver homogenates, when injected intraperitoneally, can recruit large numbers of immune cells. Among these immune cells were activated eosinophils. While eosinophils are well known to accumulate in the lungs of asthmatics or in response to helminths and parasites, several studies have shown the presence of eosinophils in liver biopsies of drug-induced liver injury, primary biliary cirrhosis, chronic hepatitis C, hepatic allograft rejection, and liver fibrosis. The prevalence of eosinophilic infiltrates in the liver points to a correlation between infiltration and disease outcome. Our results demonstrated eosinophil activation upon exposure to necrotic liver components. Exposure to necrotic liver cells induced eosinophil degranulation as measured by expression of CD107a and eosinophil peroxidase release into the supernatant as measured by ELISA. Further study of eosinophil activation during necrotic liver exposure showed IL-1β and IL-18 release as well as cell death. All of these responses were dependent upon caspase-1 activation. Caspase-1 mediated cell death accompanied by IL-1β and IL-18 release are hallmarks of pyroptosis, an inflammatory cell death pathway. We verified eosinophil pyroptosis in vivo using a liver fibrosis model involving Schistosoma mansoni infected mice. Eosinophils extracted from S. mansoni infected livers showed caspase-1 activation and cytokine release indicating that these cells undergo pyroptosis in vivo in response to hepatocyte injury.
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Macapagal, Daphne, Jane Connor, Thirumalai R. Ramalingam, Thomas A. Wynn, Tomas Mikael Mustelin, and Todd S. Davidson. "Necrotic liver induces pyroptosis through Caspase-1 in eosinophils." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 56.1. http://dx.doi.org/10.4049/jimmunol.196.supp.56.1.
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Abstract During sterile inflammatory reactions damage associated molecular patterns (DAMPS) are released from necrotic cells and recruit immune cells to the sites of tissue injury. We found that necrotic liver homogenates, when injected intraperitoneally, can recruit large numbers of immune cells. Among these immune cells were activated eosinophils. Eosinophils are polymorphonuclear leukocytes typically found within tissues of the gastrointestinal and respiratory tracts. While eosinophils are well known to accumulate in the lungs of asthmatics or in response to helminths and parasites, several studies have shown the presence of eosinophils in liver biopsies of drug-induced liver injury, chronic hepatitis C and liver fibrosis. The prevalence of eosinophilic infiltrates in the liver points to a correlation between infiltration and disease outcome. Our results demonstrated eosinophil activation upon exposure to necrotic liver components. Exposure to necrotic liver cells induced eosinophil degranulation as measured by expression of CD107a and eosinophil peroxidase release as measured by ELISA. Further study of eosinophil activation during necrotic liver exposure showed IL-1β and IL-18 release as well as cell death. All of these responses were dependent upon caspase-1 activation. Caspase-1 mediated cell death accompanied by IL-1β and IL-18 release are hallmarks of pyroptosis, an inflammatory cell death pathway. We verified eosinophil pyroptosis in vivo using a liver fibrosis model involving Schistosoma mansoni infected mice. Eosinophils extracted from S. mansoni infected livers showed caspase-1 activation and cytokine release indicating that these cells undergo pyroptosis in vivo in response to hepatocyte injury.
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Patnode, Michael L., Jennifer K. Bando, Matthew F. Krummel, Richard M. Locksley, and Steven D. Rosen. "Leukotriene B4 amplifies eosinophil accumulation in response to nematodes." Journal of Experimental Medicine 211, no. 7 (June 2, 2014): 1281–88. http://dx.doi.org/10.1084/jem.20132336.
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Eosinophil accumulation is a defining feature of the immune response to parasitic worm infection. Tissue-resident cells, such as epithelial cells, are thought to initiate eosinophil recruitment. However, direct recognition of worms by eosinophils has not been explored as a mechanism for amplifying eosinophil accumulation. Here, we report that eosinophils rapidly migrate toward diverse nematode species in three-dimensional culture. These include the mammalian parasite Nippostrongylus brasiliensis and the free-living nematode Caenorhabditis elegans. Surprisingly, collective migration toward worms requires paracrine leukotriene B4 signaling between eosinophils. In contrast, neutrophils show a minimal response to nematodes, yet are able to undergo robust leukotriene-dependent migration toward IgG-coated beads. We further demonstrate that eosinophils accumulate around C. elegans in the lungs of mice. This response is not dependent on bacterial products, CCR3, or complement activation. However, mice deficient in leukotriene signaling show markedly attenuated eosinophil accumulation after injection of C. elegans or N. brasiliensis. Our findings establish that nematode-derived signals can directly induce leukotriene production by eosinophils and that leukotriene signaling is a major contributor to nematode-induced eosinophil accumulation in the lung. The similarity of the eosinophil responses to diverse nematode species suggests that conserved features of nematodes are recognized during parasite infection.
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Tsarev, Sergey V. "Eosinophilic pneumonia in allergological practice." Russian Journal of Allergy 18, no. 1 (March 15, 2021): 32–40. http://dx.doi.org/10.36691/rja1413.
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In this article, current data on pulmonary eosinophilia are presented. Pulmonary eosinophilia is defined as the infiltration of eosinophils into the airways, interstitia, and alveoli. There are diverse processes in etiology, the common feature of which is the presence of pulmonary eosinophilic infiltrates, and as a rule, peripheral blood eosinophilia. Causes of pulmonary eosinophilia include various infections, medications, parasites, autoimmune processes, malignancies, and presence of obstructive pulmonary diseases. A unified classification of pulmonary eosinophilia is lacking, and instead, various versions of classifications have been presented. The most convenient classification option for use is also distinguished. This article discusses the historical transformation of the term eosinophilic pneumonia in the field of allergology, showing the lack of unambiguity in the concept of eosinophilic pneumonia, as well as the location of eosinophilic pneumonia in the pulmonary eosinophilia section. Eosinophilic pneumonia is defined as a disease characterized by an increase in the eosinophil content in the pulmonary tissue or bronchoalveolar lavage fluid. Most eosinophilic pneumonias are associated with peripheral blood eosinophilia. Two main variants of the disease are acute and chronic eosinophilic pneumonias. Thus, various ways to formulate diagnoses in various cases of eosinophilic pneumonia have been proposed.
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Park, Sunghee, Jiwon Jung, Yong Pil Chong, Sung-Han Kim, Sang-Oh Lee, Sang-Ho Choi, Yang Soo Kim, and Min Jae Kim. "Infectious Causes of Eosinophilic Meningitis in Korean Patients: A Single-Institution Retrospective Chart Review from 2004 to 2018." Korean Journal of Parasitology 59, no. 3 (June 21, 2021): 227–33. http://dx.doi.org/10.3347/kjp.2021.59.3.227.
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Eosinophilic meningitis is defined as the presence of more than 10 eosinophils per μl in the cerebrospinal fluid (CSF), or eosinophils accounting for more than 10% of CSF leukocytes in patients with acute meningitis. Parasites are the most common cause of eosinophilic meningitis worldwide, but there is limited research on patients in Korea. Patients diagnosed with eosinophilic meningitis between January 2004 and June 2018 at a tertiary hospital in Seoul, Korea were retrospectively reviewed. The etiology and clinical characteristics of each patient were identified. Of the 22 patients included in the study, 11 (50%) had parasitic causes, of whom 8 (36%) were diagnosed as neurocysticercosis and 3 (14%) as Toxocara meningitis. Four (18%) patients were diagnosed with fungal meningitis, and underlying immunodeficiency was found in 2 of these patients. The etiology of another 4 (18%) patients was suspected to be tuberculosis, which is endemic in Korea. Viral and bacterial meningitis were relatively rare causes of eosinophilic meningitis, accounting for 2 (9%) and 1 (5%) patients, respectively. One patient with neurocysticercosis and 1 patient with fungal meningitis died, and 5 (23%) had neurologic sequelae. Parasite infections, especially neurocysticercosis and toxocariasis, were the most common cause of eosinophilic meningitis in Korean patients. Fungal meningitis, while relatively rare, is often aggressive and must be considered when searching for the cause of eosinophilic meningitis.
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Gopinath, Ramya, L. E. Hanna, V. Kumaraswami, V. Perumal, V. Kavitha, V. Vijayasekaran, and Thomas B. Nutman. "Perturbations in Eosinophil Homeostasis following Treatment of Lymphatic Filariasis." Infection and Immunity 68, no. 1 (January 1, 2000): 93–99. http://dx.doi.org/10.1128/iai.68.1.93-99.2000.
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ABSTRACT Treatment of patients with patent Wuchereria bancroftiinfection results in an acute clinical reaction and peripheral eosinophilia. To investigate the dynamics of the eosinophil response, changes in eosinophil activation and degranulation and plasma levels of eosinophil-active chemokines and cytokines were studied in 15 microfilaremic individuals in south India by sequential blood sampling before and after administration of 300 mg of diethylcarbamazine (DEC). Clinical symptoms occurred within 24 h. Plasma interleukin-5 (IL-5) and RANTES levels peaked 1 to 2 days posttreatment, preceding a peak peripheral eosinophil count at day 4. Major basic protein secretion from eosinophils paralleled IL-5 secretion, while levels of eosinophil-derived neurotoxin peaked at day 13 after treatment. Expression of the activation markers HLA-DR and CD25 on eosinophils rose markedly immediately after treatment, while expression of VLA-4 and α4β7 showed an early peak within 24 h and a second peak at day 13. Thus, the posttreatment reactions seen in filarial infections can be divided into an early phase with killing of microfilariae, clinical symptomatology, increases in plasma IL-5 and RANTES levels, and eosinophil activation and degranulation and a later phase with expression of surface integrins on eosinophils, recruitment of eosinophils from the bone marrow to tissues, and clearance of parasite antigen.
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Negrão-Corrêa, Deborah, Micheline R. Silveira, Cynthia M. Borges, Danielle G. Souza, and Mauro M. Teixeira. "Changes in Pulmonary Function and Parasite Burden in Rats Infected with Strongyloides venezuelensis Concomitant with Induction of Allergic Airway Inflammation." Infection and Immunity 71, no. 5 (May 2003): 2607–14. http://dx.doi.org/10.1128/iai.71.5.2607-2614.2003.
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ABSTRACT The prevalence of allergic diseases such as asthma has increased markedly over the past few decades. To evaluate the possible mutual influence of helminth infection and allergy, the combined effects of experimental allergic airway inflammation and infection with Strongyloides venezuelensis on various parasitological and inflammatory indices were evaluated in the rat. A challenge of immunized rats with aerosolized ovalbumin (OVA) resulted in eosinophilic inflammation that peaked 48 h after the challenge and was accompanied by airway hyperresponsiveness (AHR) to an intravenous acetylcholine challenge. S. venezuelensis infection concomitant with an OVA challenge of immunized rats resulted in prolonged pulmonary inflammation with increased eosinophil infiltration in bronchoalveolar lavage fluid but not in the lung tissue. These rats also showed a significant parasite burden reduction, especially during parasite migration through the lungs. However, the fecundity rates of worms that reached the intestine were similar in allergic and nonallergic animals. Despite airway inflammation, the increased responsiveness of the airways in the experimental asthma model was suppressed during parasite migration through the lungs (2 days). In contrast, parasite-induced AHR was unchanged 5 days after infection in immunized and challenged rats. In conclusion, infection with S. venezuelensis interfered with the onset of AHR following an antigen challenge of immunized rats. The ability of parasites to switch off functional airway responses is therapeutically relevant because we may learn from parasites how to modulate lung function and, hence, the AHR characteristic of asthmatic patients.
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Nogueira, Denise Silva, Luciana Maria de Oliveira, Chiara Cássia Oliveira Amorim, Ana Clara Gazzinelli-Guimarães, Fernando Sérgio Barbosa, Fabrício Marcus Silva Oliveira, Lucas Kraemer, et al. "Eosinophils mediate SIgA production triggered by TLR2 and TLR4 to control Ascaris suum infection in mice." PLOS Pathogens 17, no. 11 (November 16, 2021): e1010067. http://dx.doi.org/10.1371/journal.ppat.1010067.
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Human ascariasis is the most prevalent but neglected tropical disease in the world, affecting approximately 450 million people. The initial phase of Ascaris infection is marked by larval migration from the host’s organs, causing mechanical injuries followed by an intense local inflammatory response, which is characterized mainly by neutrophil and eosinophil infiltration, especially in the lungs. During the pulmonary phase, the lesions induced by larval migration and excessive immune responses contribute to tissue remodeling marked by fibrosis and lung dysfunction. In this study, we investigated the relationship between SIgA levels and eosinophils. We found that TLR2 and TLR4 signaling induces eosinophils and promotes SIgA production during Ascaris suum infection. Therefore, control of parasite burden during the pulmonary phase of ascariasis involves eosinophil influx and subsequent promotion of SIgA levels. In addition, we also demonstrate that eosinophils also participate in the process of tissue remodeling after lung injury caused by larval migration, contributing to pulmonary fibrosis and dysfunction in re-infected mice. In conclusion, we postulate that eosinophils play a central role in mediating host innate and humoral immune responses by controlling parasite burden, tissue inflammation, and remodeling during Ascaris suum infection. Furthermore, we suggest that the use of probiotics can induce eosinophilia and SIgA production and contribute to controlling parasite burden and morbidity of helminthic diseases with pulmonary cycles.
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Yamaguchi, Y., T. Suda, J. Suda, M. Eguchi, Y. Miura, N. Harada, A. Tominaga, and K. Takatsu. "Purified interleukin 5 supports the terminal differentiation and proliferation of murine eosinophilic precursors." Journal of Experimental Medicine 167, no. 1 (January 1, 1988): 43–56. http://dx.doi.org/10.1084/jem.167.1.43.
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Using a clonal culture system, we investigated the hemopoietic effects of purified recombinant IL-5 obtained from conditioned media of transfected Xenopus oocytes. IL-5 alone acted on untreated bone marrow cells and supported the formation of a small number of colonies, all of which were predominantly eosinophilic. However, it did not support colony formation by spleen cells from 5-FU-treated mice, in which only primitive stem cells had survived, while IL-3 and G-CSF did. Eosinophil-containing colonies were formed from these cells in the presence of IL-5 and G-CSF together. In contrast, G-CSF alone did not support any eosinophil colonies. The eosinophilopoietic effect of IL-5 was dose-dependent, and was neutralized specifically by anti-IL-5 antibody. To exclude the possibility of interactions with accessory cells in the same culture dish, we replated a small number (200 cells/dish) of enriched hemopoietic progenitors, obtained from blast cell colonies, which were formed by cultivation of spleen cells from 5-FU-treated mice in the presence of IL-3 or G-CSF. From these replated blast cells, eosinophil colonies were induced in dishes containing IL-5 but not in those containing G-CSF alone. From these findings, it was concluded that IL-5 did not act on primitive hemopoietic cells, but on blast cells induced by IL-3 or G-CSF. IL-5 specifically facilitated the terminal differentiation and proliferation of eosinophils. In this respect, the role of IL-5 in eosinophilopoiesis seems to be analogous to erythropoietin, which promotes the terminal differentiation and amplification of erythroid cells. Moreover, IL-5 maintained the viability of mature eosinophils obtained from peritoneal exudate cells of the mice infected with parasites, indicating mature functional eosinophils carried IL-5 receptors. The synergistic effects of IL-5 and colony-stimulating factors on the expansion of eosinophils is supposed to contribute to the urgent mobilization of eosinophils at the time of helminthic infections and allergic responses.
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Dent, L. A., M. Strath, A. L. Mellor, and C. J. Sanderson. "Eosinophilia in transgenic mice expressing interleukin 5." Journal of Experimental Medicine 172, no. 5 (November 1, 1990): 1425–31. http://dx.doi.org/10.1084/jem.172.5.1425.
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Experiments in vitro suggest that although interleukin 5 (IL-5) stimulates the late stages of eosinophil differentiation, other cytokines are required for the generation of eosinophil progenitor cells. In this study transgenic mice constitutively expressing the IL-5 gene were established using a genomic fragment of the IL-5 gene coupled to the dominant control region from the gene encoding human CD2. Four independent eosinophilic transgenic lines have thus far been established, two of which with 8 and 49 transgene copies, are described in detail. These mice appeared macroscopically normal apart from splenomegaly. Eosinophils were at least 65- and 265-fold higher in blood from transgenics, relative to normal littermates, and approximately two- or sevenfold more numerous relative to blood from mice infected with the helminth Mesocestoides corti. Much more modest increases in blood neutrophil, lymphocyte, and monocyte numbers were noted in transgenics, relative to normal littermates (less than threefold). Thus IL-5 in vivo is relatively specific for the eosinophil lineage. Large numbers of eosinophils were present in spleen, bone marrow, and peritoneal exudate, and were highest in the line with the greatest transgene copy number. Eosinophilia was also noted in histological sections of transgenic lungs, Peyer's patches, mesenteric lymph nodes, and gut lamina propria but not in other tissues examined. IL-5 was detected in the sera of transgenics at levels comparable to those seen in sera from parasite-infected animals. IL-3 and granulocyte/macrophage colony-stimulating factor (GM-CSF) were not found. IL-5 mRNA was detected in transgenic thymus, Peyer's patches, and superficial lymph nodes, but not in heart, liver, brain, or skeletal muscle or in any tissues from nontransgenics. Bone marrow from transgenic mice was rich in IL-5-dependent eosinophil precursors. These data indicate that induction of the IL-5 gene is sufficient for production of eosinophilia, and that IL-5 can induce the full pathway of eosinophil differentiation. IL-5 may therefore not be restricted in action to the later stages of eosinophil differentiation, as suggested by earlier in vitro studies.
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Herndon, F. J., and S. G. Kayes. "Depletion of eosinophils by anti-IL-5 monoclonal antibody treatment of mice infected with Trichinella spiralis does not alter parasite burden or immunologic resistance to reinfection." Journal of Immunology 149, no. 11 (December 1, 1992): 3642–47. http://dx.doi.org/10.4049/jimmunol.149.11.3642.
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Abstract Mechanisms of parasite killing by eosinophils are widely studied and are often implicated in mediating resistance to parasitic infection, especially in conjunction with specific antibodies. Evidence for the eosinophil as an anti-parasite killer cell in vivo is limited and may not justify the belief that eosinophils engage and/or kill infective helminths. We reexamined this question in a mouse model of trichinosis in which antisera to eosinophils were previously used to show the requirement for eosinophils in resistance to this nematode. The current studies used mAb to IL-5 to suppress eosinophil levels in CF1 mice infected with Trichinella spiralis. In mice given a primary infection and injected with an isotype control mAb or left untreated, the medullary and peripheral blood eosinophil numbers peaked at 3 wk postinfection (PI) and returned to baseline levels by 4 wk PI. Peripheral blood eosinophil numbers in infected mice injected with anti-IL-5 were maintained at levels below those of uninfected normal mice through 4 wk of infection. Histologically, there was a prominent eosinophil accumulation in infected, untreated, or control-mAb-treated mice associated with nurse cell complexes containing infective juveniles in skeletal muscle at 3 and 4 wk PI. This was largely eliminated in mice treated with anti-IL-5 mAb. However, the number of muscle stage juvenile worms recovered 3 and 4 wk PI after acid pepsin digestion was unaffected by eosinophil depletion. Challenge infections, in which mice were infected at day 0 with 125 muscle stage worms and challenged at day 28 PI with 350 muscle stage worms, developed peak eosinophil numbers in bone marrow and peripheral blood 3 wk after primary infection and 2 wk after challenge infection in mice receiving either no treatment or control mAb. In challenged mice receiving anti-IL-5 mAb, medullary and peripheral blood eosinophil numbers remained at or below those of uninfected animals. Although all groups exhibited significant resistance measured as muscle stage worm burdens 56 days PI, eosinophil depletion did not affect resistance of muscle worm recovery. These results suggest that eosinophils are not essential in the control of T. spiralis in either primary or challenge infections of CF1 mice. This in vivo study illustrates the questionable value of in vitro killing assays to assign effector function to any single inflammatory cell type.
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Ansari, Rehan, Elva Nora Osuna Salazar, Nabeel Sarhill, Laura E. Garcia, and James Hanley. "All Itching Is Not Benign; A Case of Refractory Hypereosinophilic Syndrome Treated with Off Label CD52 Inhibitor-Alemtuzumab." Blood 132, Supplement 1 (November 29, 2018): 5485. http://dx.doi.org/10.1182/blood-2018-99-118271.
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Abstract INTRODUCTION Usually attributed to allergies or parasites (Seifert et. al Medline 2008) eosinophila is often overlooked. However hypereosinophilia (absolute eosinophil count >1.5 X 109/L on two separate exams one month apart or with pathologic confirmation) can have serious manifestations. When hypereosinophilia is associated with eosinophil-mediated organ damage or dysfunction, a hypereosinophilic syndrome (HES) exists. With an unpredictable course, eosinophilic infiltration commonly affects the skin (eczema), lung (dyspnea), & GIT (gastritis). However life-threatening damage to the CVS (myocarditis) or the CNS may occur. Clinically HES is subdivided into: myeloid variants (M-HES), T lymphocytic variants (L-HES), Familial HES, Idiopathic HES, Organ-restricted, and specific/defined syndromes associated with hypereosinophilia (Roufosse et. al Respiration 2016). Treatment is based upon symptoms and the molecular presence of Fip1-like1-platelet-derived growth factor receptor alpha. If present, patients are initially treated with imatinib mesylate, while those with other types are given a trial of steroids (Cools et. al N Engl J Med 2003). Regrettably complete remissions are rare and long term corticosteroid uses are infamous. Corticosteroid-refractory HES can be fatal with a reported 10 year survival of <50% (Verstovsek, S et. al Clinical Cancer Res 2009). Options are limited for non-responders or recurrence. We present a patient that successfully reached clinical & pathological remission after treatment with alemtuzumab, an anti CD-52 monoclonal antibody. CASE A 71y/o M with a history of COPD complained of localized pruritus to his back that improved with antihistamines and topical steroids. After a few years he started to experience deterioration in his symptoms and was found to have eosinophilia. Any attempts to taper his oral steroids lead to a widespread manifestation of pruritus and lichenification. At the Mayo Clinic a comprehensive workup was performed including a bone marrow and skin biopsy that revealed perivascular and interstitial mixed dermal inflammation with eosinophils. He had an absolute eosinophil count of 6.92 X 109/L (N<0.5 x 109/L). FISH and 2,3-dinor 11B-Prostaglandin F2a, U levels were within normal limits. Serology was negative for multiple bacteria and parasites. A bronchoalveolar lavage revealed increased levels of eosinophils, concerning for lung involvement. Between mepolizumab, an anti IL-5 humanized monoclonal antibody used in severe eosinophilic asthmatics and alemtuzumab, insurance approved of the latter. After 12 treatments he reached complete remission and resolution of symptoms with a normal blood eosinophil level of 0.1 X 103/uL. A repeat bone marrow biopsy did not reveal any primary hematolymphoid neoplasm. DISCUSSION Alemtuzumab is a monoclonal antibody that targets CD 52, a cell surface glycoprotein present on T and B lymphocytes, monocytes and eosinophils. Approved for use on B-cell chronic lymphocytic leukemia and relapsing multiple sclerosis, the use of alemtuzumab on HES is justified by the evidence that CD52 is highly expressed on eosinophils but is notably absent on neutrophils and bone marrow precursors (Verstovsek, S et. al Clinical Cancer Res 2009). Prior studies have been promising regarding the efficacy of alemtuzumab and HES. Out of 12 patients that were followed for 3 years, 10 achieved complete hematologic response - defined as normalization of the absolute eosinophil count (Strati, P. et. al Clinical Lymphoma, Myeloma & Leukemia 2012). Adverse effects have been related to the infusion (fever), and lymphopenia. There is an increased risk of opportunistic infections, especially CMV. Late complications such as secondary lymphomas may also develop. Close follow up and appropriate prophylaxis can be used to mitigate these complications. CONCLUSION Our patient responded well to alemtuzumab, without any notable side effects. Therapy should be reserved due to early and late adverse affects but this agent has proved to be an effective treatment for HES in terms of both complete hematologic response and duration (Strati, P. et. al Clinical Lymphoma, Myeloma & Leukemia 2012). Moreover resistance is not seen, as patients with relapse were able to achieve a second remission. Data about efficacy and safety in the long-term remains lacking, but for treatment resistant and refractory HES, Alemtuzmab may be a suitable choice. Disclosures No relevant conflicts of interest to declare.
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Vallance, Bruce A., Patricia A. Blennerhassett, Yikang Deng, Klaus I. Matthaei, Ian G. Young, and Stephen M. Collins. "IL-5 contributes to worm expulsion and muscle hypercontractility in a primaryT. spiralisinfection." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 2 (August 1, 1999): G400—G408. http://dx.doi.org/10.1152/ajpgi.1999.277.2.g400.
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Enteric nematode infections lead to increased interleukin (IL)-5 expression, eosinophilic inflammation, and intestinal smooth muscle hypercontractility. Although eosinophils release inflammatory mediators that cause smooth muscle contraction, the role of IL-5 and eosinophils in enteric smooth muscle hypercontractility is unclear. IL-5-deficient mice and their wild-type controls were infected with the nematode Trichinella spiralis. Intestinal parasites and eosinophils were counted, and jejunal longitudinal muscle contractility was assessed. During infection, IL-5 gene expression increased significantly in wild-type mice and was accompanied by significant intestinal eosinophilia in wild-type but not IL-5-deficient mice. Although both strains developed increased muscle contractility during infection, contraction was significantly less in the IL-5-deficient mice at days 16 and 21 postinfection. In addition, parasite expulsion was transiently delayed at day 16 in IL-5-deficient mice. Thus, in the nematode-infected mouse, IL-5 appears essential for intestinal eosinophilia and contributes to, but is not essential for, the development of muscle hypercontractility. IL-5 also appears to play a minor role in expelling a primary T. spiralis infection from the gut.
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Zoll, Whitney M., Dhani Prakoso, Michael Dark, Junjie Liu, Heather Stockdale-Walden, and Maureen T. Long. "Histologic characterization of eosinophilic encephalitis in horses in Florida." Journal of Veterinary Diagnostic Investigation 30, no. 3 (March 12, 2018): 442–46. http://dx.doi.org/10.1177/1040638718763877.
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Eosinophils within the central nervous system are abnormal and are usually associated with fungal or parasitic infections in horses. Causative agents include Halicephalobus gingivalis, Sarcocystis neurona, and Neospora hughesi. Confirmation of these organisms via specific testing is typically not performed, and final diagnoses are often presumptive. With molecular technology, many of these organisms can now be confirmed. This is important for emerging and zoonotic pathogens, including Angiostrongylus cantonensis, an emerging parasite of interest in the southeastern United States. We retrospectively analyzed eosinophilic encephalitides in Floridian horses for H. gingivalis, S. neurona, and A. cantonensis, applied descriptors to equine eosinophilic encephalitides, and determined if a relationship existed between these descriptions and specific etiologic agents. In a database search for horses with eosinophilic and other encephalitides submitted to the University of Florida, College of Veterinary Medicine, Anatomic Pathology Service, we identified 27 horses with encephalitis, and performed DNA isolation and rtPCR on formalin-fixed, paraffin-embedded blocks from these cases. Real-time PCR identified 6 horses positive for S. neurona and 4 horses positive for H. gingivalis; all horses were negative for A. cantonensis. All 25 control horses were negative for H. gingivalis, S. neurona, and A. cantonensis. Pattern analysis and eosinophil enumeration were not useful in differentiating among causes of eosinophilic encephalitides in horses in our study.
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Park, Sunghee, Jiwon Jung, Yong Pil Chong, Sung-Han Kim, Sang-Oh Lee, Sang-Ho Choi, Yang Soo Kim, Jun Hee Woo, and Min Jae Kim. "348. Etiology of Eosinophilic Meningitis in Korea." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S244. http://dx.doi.org/10.1093/ofid/ofaa439.543.
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Abstract Background Eosinophilic meningitis is defined as the presence of more than 10 eosinophils per mm3 in the cerebrospinal fluid (CSF), or eosinophils accounting for more than 10 percent of CSF leukocytes in a patient with symptoms or signs suggestive of acute meningitis. Parasites are known to be the most common cause of eosinophilic meningitis worldwide, but there is limited research on patients in South Korea. Methods We retrospectively reviewed patients with eosinophilic meningitis at a tertiary hospital in Seoul, South Korea, from 2004 to 2018. Patients who were suspected of having a non-infectious cause were excluded. Etiology and clinical characteristics such as age, sex, risk factors, symptoms and signs, laboratory and radiologic findings, treatment, and prognosis were identified. Results Of the 35 patients included in this study, 11 (31.4%) had parasitic causes, with 8 (22.9%) diagnosed as neurocysticercosis, and 3 (8.6%) as toxocara meningitis. Four (11.4%) were diagnosed with fungal meningitis, and underlying immunodeficiency was found in 2 of these patients. Tuberculous meningitis was suspected in 4 (11.4%), while viral and bacterial meningitis were rare causes of eosinophilic meningitis, with 2 (5.7%) and 1 (2.9%) patients, respectively. One patient with neurocysticercosis and one patient with fungal meningitis died, while 8 (22.9%) had remaining neurologic sequelae. The etiology was unknown in 13 patients (37.1%). Four of these patients received empirical anti-tuberculosis therapy, while 5 were treated empirically with acyclovir. Conclusion Parasite infections, especially neurocysticercosis and toxocariasis, were the most common cause of eosinophilic meningitis in South Korean patients. Fungal meningitis, while relatively rare, is often aggressive and should always be considered when searching for the cause of eosinophilic meningitis. Disclosures All Authors: No reported disclosures
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Magrone, Thea, Manrico Magrone, and Emilio Jirillo. "Eosinophils, a Jack of All Trades in Immunity: Therapeutic Approaches for Correcting Their Functional Disorders." Endocrine, Metabolic & Immune Disorders - Drug Targets 20, no. 8 (October 15, 2020): 1166–81. http://dx.doi.org/10.2174/1871530320666200309094726.
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Background: Eosinophils are primitive myeloid cells derived from bonemarrow precursors and require the intervention of interleukin (IL)-5 for their survival and persistence in blood and tissues. Under steady-state conditions, they contribute to immune regulation and homeostasis. Under pathological circumstances, eosinophils are involved in host protection against parasites and participate in allergy and inflammation. Discussion: Mostly, in asthma, eosinophils provoke airway damage via the release of granule contents and IL-13 with mucus hypersecretion and differentiation of goblet cells. Then, tissue remodeling follows with the secretion of transforming growth factor-β. Eosinophils are able to kill helminth larvae acting as antigen-presenting cells with the involvement of T helper (h)-2 cells and subsequent antibody response. However, they also exert pro-worm activity with the production of suppressive cytokine (IL- 10 and IL-4) and inhibition of nitric oxide. Eosinophils may play a pathogenic role in the course of chronic and autoimmune disease, e.g., inflammatory bowel disease and eosinophilic gastroenteritis, regulating Th2 responses and promoting a profibrotic effect. In atopic dermatitis, eosinophils are commonly detected and may be associated with disease severity. In cutaneous spontaneous urticaria, eosinophils participate in the formation of wheals, tissue remodeling and modifications of vascular permeability. With regard to tumor growth, it seems that IgE can exert anti-neoplastic surveillance via mast cell and eosinophil-mediated cytotoxicity, the so-called allergo-oncology. From a therapeutic point of view, monoclonal antibodies directed against IL-5 or the IL-5 receptors have been shown to be very effective in patients with severe asthma. Finally, as an alternative treatment, polyphenols for their anti-inflammatory and anti-allergic activities seem to be effective in reducing serum IgE and eosinophil count in bronchoalveolar lavage in murine asthma. Conclusion: Eosinophils are cells endowed with multiple functions and their modulation with monoclonal antibodies and nutraceuticals may be effective in the treatment of chronic disease.
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Zhu, Qing, Christopher W. Thomson, Guofeng Zhang, Martin Stämpfli, Mark R. McDermott, Stephen M. Collins, and Jack Gauldie. "Eosinophilia is induced in the colon of Th2-sensitized mice upon exposure to locally expressed antigen." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 1 (July 2007): G383—G390. http://dx.doi.org/10.1152/ajpgi.00341.2006.
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Eosinophilic inflammation is a feature of a variety of gastrointestinal (GI) disorders including eosinophil-associated GI disorder, allergy, inflammatory bowel disease, and parasite infection. Elucidating the mechanisms of eosinophil infiltration into the GI tract is important to the understanding of multiple disease processes. We hypothesize that eosinophilia in the large intestine (colon) can be induced by an antigen in a host that is associated with Th2-skewed antigen-specific immune responses. To investigate the importance of antigenic triggering, we established polarized antigen-specific Th2 type responses in BALB/c mice, using ovalbumin in conjunction with aluminum hydroxide. Upon challenge at the colonic mucosa through transient (3–4 days) expression of the antigen gene encoded in an adenovirus vector, sensitized animals developed significant subepithelial colonic inflammation, characterized by marked eosinophilic infiltration, and the presence of enlarged and increased numbers of lymphoid follicles. The alterations peaked around day 5 and resolved over the next 5–10 days, and no epithelial cell damage was detected through the entire course. Administration of a control (empty) adenovirus vector did not lead to any pathological changes. These data suggest that colonic eosinophilia can be induced by exposure to an antigen associated with preexisting Th2-skewed responses. Thus the model established here may provide a useful tool to study GI and, in particular, colonic inflammation with respect to underlying mechanisms involved in the recruitment and the immediate function of eosinophils.
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Swartz, Jonathan M., Kimberly D. Dyer, Allen W. Cheever, Thirumalai Ramalingam, Lesley Pesnicak, Joseph B. Domachowske, James J. Lee, et al. "Schistosoma mansoni infection in eosinophil lineage–ablated mice." Blood 108, no. 7 (October 1, 2006): 2420–27. http://dx.doi.org/10.1182/blood-2006-04-015933.
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AbstractWe explore the controversial issue of the role of eosinophils in host defense against helminthic parasites using the established Schistosoma mansoni infection model in 2 novel mouse models of eosinophil lineage ablation (ΔdblGATA and TgPHIL). No eosinophils were detected in bone marrow of infected ΔdblGATA or TgPHIL mice, despite the fact that serum IL-5 levels in these infected mice exceeded those in infected wild type by approximately 4-fold. Liver granulomata from infected ΔdblGATA and TgPHIL mice were likewise depleted of eosinophils compared with those from their respective wild types. No eosinophil-dependent differences in granuloma number, size, or fibrosis were detected at weeks 8 or 12 of infection, and differential accumulation of mast cells was observed among the ΔdblGATA mice only at week 12. Likewise, serum levels of liver transaminases, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) increased in all mice in response to S mansoni infection, with no eosinophil-dependent differences in hepatocellular damage observed. Finally, eosinophil ablation had no effect on worm burden or on egg deposition. Overall, our data indicate that eosinophil ablation has no impact on traditional measures of disease in the S mansoni infection model in mice. However, eosinophils may have unexplored immunomodulatory contributions to this disease process.
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Sivaram, M., A. White, and K. W. Radcliffe. "Eosinophilia: clinical significance in HIV-infected individuals." International Journal of STD & AIDS 23, no. 9 (September 2012): 635–38. http://dx.doi.org/10.1258/ijsa.2012.011409.
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This study was conducted to determine the relationship between eosinophilia and parasitic infection in HIV-infected individuals. HIV-positive patients attending an HIV clinic in Birmingham were recruited and classified as either eosinophilic (>400 eosinophils/mm3) or non-eosinophilic. A demographic and parasitic risk history was taken and clinical examination was performed. Urine and stool were examined for parasites, and blood samples taken for parasite serology. A total of 266 patients (96 eosinophilic and 170 non-eosinophilic) were recruited. Of 64 eosinophilic patients who had a stool examination, one (1.6%) was positive for both Strongyloides larvae and schistosomal eggs. Urine microscopy was negative in the 245 patients (88 eosinophilic, 157 non-eosinophilic) from whom a sample was available. Two hundred and sixty-three patients underwent serological investigation (96 eosinophilic and 167 non-eosinophilic): 13 (4.9%) were positive for schistosomiasis and three (1.1%) positive for Strongyloides. A significant association between eosinophilia and positive schistosomal serology was found ( P = 0.003): 11 (10.5%) were eosinophilic patients, while only four (2.3%) were non-eosinophilic patients. Eosinophilia was associated with a low nadir CD4 count ( P = 0.021) and prior AIDS-defining illness ( P = 0.041). In all, 7.8% of patients from a developing country and 5.3% of patients from a developed country with a travel history had positive parasitic serology. Eosinophilia in HIV-infected patients was significantly associated with positive serology for schistosomiasis, low nadir CD4 count and prior AIDS-defining illness. Geographical exposure is also an important determinant of positive parasitic serology.
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Kurniawan, Roy Bagus, Puspa Wardhani, Heny Arwati, Aryati Aryati, Trieva Verawaty Butarbutar, Christophorus Oetama Adiatmaja, Amarensi Milka Betaubun, and Nur Chamidah. "Association of Parasite Density and Hematological Parameters of Plasmodium vivax- and Plasmodium falciparum-infected Patients Attending Merauke General Hospital, Papua, Indonesia." Open Access Macedonian Journal of Medical Sciences 8, B (October 10, 2020): 825–31. http://dx.doi.org/10.3889/oamjms.2020.4881.
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BACKGROUND: Plasmodium falciparum and Plasmodium vivax are frequent causes of malaria. Although they are blood parasites, their biological characteristics are dissimilar, and their species-related consequences on hematological parameters have not been widely investigated. They might be valuable to distinguish both species infection, notably for an endemic region with limited diagnostic resources.
AIM: This study aimed to know the species-specific effect on hematological parameters and its correlation to the parasite density in P. vivax- and P. falciparum-infected patients attending Merauke General Hospital, Papua, Indonesia.
MATERIALS AND METHODS: Malaria patients confirmed by blood film microscopy from January 1 to July 31, 2019, were recruited, and their hematological parameters were measured using Sysmex XN-1000 instrument. All obtained data were analyzed statistically.
RESULTS: From 100 malaria-positive patients, 87 patients, consisting of 57 P. vivax and 30 P. falciparum patients, met criteria. Anemia and parasite density >50,000 parasites/μL were significantly higher in P. falciparum than P. vivax patients (p < 0.05) though hemoglobin concentration and parasite density were insignificantly different. Interestingly, basophil count was significantly higher in P. falciparum compared to P. vivax patients (p = 0.04). The eosinophil count was significantly higher in P. vivax (p = 0.01) than P. falciparum patients and indicated a significant positive correlation (p = 0.04, r = +0.28) with the parasite density.
CONCLUSION: There were significant differences between basophil and eosinophil count between P. vivax and P. falciparum infections. Eosinophil count showed a significant positive correlation with parasite density.
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Niwa, A., K. Asano, and A. Ito. "Eosinophil chemotactic factors from cysticercoids of Hymenolepis nana." Journal of Helminthology 72, no. 3 (September 1998): 273–75. http://dx.doi.org/10.1017/s0022149x00016552.
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AbstractA comparative study of eosinophil chemotactic factors was carried out using cysticercoids and oncospheres of Hymenolepis nana. Cysticercoids showed twice the chemotactic activity for eosinophils than the oncospheres. Eosinophilia induced by oncospheres and cysticercoids observed in secondary and primary infections, respectively, were discussed from the view point of the immunobiology of this parasite.
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Huang, Lu, Nebiat Gebreselassie, Lucille Gagliardo, Nancy Lee, James Lee, and Judith Appleton. "Eosinophils promote immune responses that preserve parasitic nematode larvae (P3086)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 125.18. http://dx.doi.org/10.4049/jimmunol.190.supp.125.18.
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Abstract We have shown that eosinophils protect, rather than attack Trichinella spiralis larvae during primary infection in the skeletal muscle. Accumulation of Th2 cells at sites of infection is also impaired in the absence of eosinophils. Here we further elucidated the mechanism underlying this effect. Intravenous infection with T. spiralis newborn larvae specifically and rapidly induced the recruitment of eosinophils to skeletal muscle. The presence of eosinophils only during the earliest stages of muscle infection was sufficient to support parasite growth and survival, suggesting that eosinophils are required to be present at the time newborn larvae first arrive in the muscle, when the local immune response is first engaged. Transfer of MHCII-/- eosinophils also supported parasite growth and survival, showing that antigen presentation by eosinophils is not required. Furthermore, the numbers of myeloid dendritic cells in cervical lymph nodes and skeletal muscles were reduced in eosinophil-ablated, infected mice and improved when eosinophils were restored. The reduction in myeloid dendritic cells correlated with decreased numbers of proliferating Th2 cells in cervical lymph nodes, indicating that eosinophils promote accumulation of myeloid dendritic cells, which may promote Th2 responses. Taken together, our findings suggest that eosinophils exert their influence at the very early stages of the immune response that preserves T. sprialis larvae.
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Hamada, A., and B. M. Greene. "Clq enhancement of IgG-dependent eosinophil-mediated killing of schistosomula in vitro." Journal of Immunology 138, no. 4 (February 15, 1987): 1240–45. http://dx.doi.org/10.4049/jimmunol.138.4.1240.
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Abstract Antibody-dependent eosinophil-mediated cytotoxicity plays a role in host protection against metazoan parasite invasion. We examined a possible role for Clq in eosinophil-mediated cytotoxicity by using a Schistosoma mansoni schistosomula killing system in vitro. The addition of monomeric purified human Clq enhanced IgG-dependent human eosinophil-mediated killing from 1.4-fold to 2.3-fold (mean percent killing 12% +/- 4 vs 21% +/- 4, p less than 0.005) when the immune IgG concentration was low. In contrast, there was no significant enhancement of neutrophil-mediated killing. When the IgG concentration was increased fourfold Clq did not cause enhancement of eosinophil-mediated killing (35% +/- 9 vs 37% +/- 5). Preincubation of eosinophils with type 1 collagen abrogated Clq enhancement of killing, raising the possibility of a receptor-mediated process, which depends upon cellular binding of Clq via the collagenous portion of the molecule. Eosinophils and neutrophils were examined for the presence of Clq receptors by using 125I labeled Clq. Clq binding to both cell types was saturable, reversible, and specific, indicating that binding is through specific receptors. Type 1 collagen inhibited binding of Clq to cells, suggesting that Clq binding is via the collagenous stalk of Clq. The number of receptors was approximately twice as high for eosinophils as compared with neutrophils (1.9 X 10(7) vs 1.1 X 10(7), p less than 0.025). Affinity constants for the two cell types were similar (1.5 X 10(7) vs 1.3 X 10(7). These findings suggest that Clq and receptors for Clq on eosinophils may be important for eosinophil-mediated schistosomula killing.
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Abraham, David, Ofra Leon, Silvia Schnyder-Candrian, Chun Chi Wang, Ann Marie Galioto, Laura A. Kerepesi, James J. Lee, and Sara Lustigman. "Immunoglobulin E and Eosinophil-Dependent Protective Immunity to Larval Onchocerca volvulus in Mice Immunized with Irradiated Larvae." Infection and Immunity 72, no. 2 (February 2004): 810–17. http://dx.doi.org/10.1128/iai.72.2.810-817.2004.
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ABSTRACT Mice immunized with irradiated Onchocerca volvulus third-stage larvae developed protective immunity. Eosinophil levels were elevated in the parasite microenvironment at the time of larval killing, and measurements of total serum antibody levels revealed an increase in the immunoglobulin E (IgE) level in immunized mice. The goal of the present study was to identify the role of granulocytes and antibodies in the protective immune response to the larval stages of O. volvulus in mice immunized with irradiated larvae. Immunity did not develop in mice if granulocytes, including both neutrophils and eosinophils, were eliminated, nor did it develop if only eosinophils were eliminated. Moreover, larvae were killed in naïve interleukin-5 transgenic mice, and the killing coincided with an increase in the number of eosinophils and the eosinophil peroxidase (EPO) level in the animals. To determine if EPO was required for protective immunity, mice that were genetically deficient in EPO were immunized, and there were no differences in the rates of parasite recovery in EPO-deficient mice and wild-type mice. Two mouse strains were used to study B-cell function; μMT mice lacked all mature B cells, and Xid mice had deficiencies in the B-1 cell population. Immunity did not develop in the μMT mice but did develop in the Xid mice. Finally, protective immunity was abolished in mice treated to eliminate IgE from the blood. We therefore concluded that IgE and eosinophils are required for adaptive protective immunity to larval O. volvulus in mice.
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Rennick, DM, L. Thompson-Snipes, RL Coffman, BW Seymour, JD Jackson, and S. Hudak. "In vivo administration of antibody to interleukin-5 inhibits increased generation of eosinophils and their progenitors in bone marrow of parasitized mice." Blood 76, no. 2 (July 15, 1990): 312–16. http://dx.doi.org/10.1182/blood.v76.2.312.312.
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Abstract Bone marrow of mice parasitized with Nippostrongylus brasiliensis showed increased numbers of eosinophils as early as 4 days after infection. By day 7, their bone marrow also contained elevated numbers of progenitors that form small eosinophil colonies (20 to 50 cells) in soft agar cultures supplemented with interleukin-5 (IL-5). However, when mice were infused with anti-IL-5 antibodies at the time of infection, the number of recognizable eosinophils present in bone marrow remained low and eventually dropped below normal levels. The antibody treatment also prevented increased generation of IL-5- responsive precursors capable of differentiating into mature eosinophils in liquid culture and inhibited the generation of progenitor cells capable of forming small eosinophil colonies or clusters in soft agar cultures. The results of these in vivo experiments directly show that IL-5 is an essential regulatory molecule required for the bone marrow-dependent phase of a parasite-induced eosinophilia.
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Rennick, DM, L. Thompson-Snipes, RL Coffman, BW Seymour, JD Jackson, and S. Hudak. "In vivo administration of antibody to interleukin-5 inhibits increased generation of eosinophils and their progenitors in bone marrow of parasitized mice." Blood 76, no. 2 (July 15, 1990): 312–16. http://dx.doi.org/10.1182/blood.v76.2.312.bloodjournal762312.
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Bone marrow of mice parasitized with Nippostrongylus brasiliensis showed increased numbers of eosinophils as early as 4 days after infection. By day 7, their bone marrow also contained elevated numbers of progenitors that form small eosinophil colonies (20 to 50 cells) in soft agar cultures supplemented with interleukin-5 (IL-5). However, when mice were infused with anti-IL-5 antibodies at the time of infection, the number of recognizable eosinophils present in bone marrow remained low and eventually dropped below normal levels. The antibody treatment also prevented increased generation of IL-5- responsive precursors capable of differentiating into mature eosinophils in liquid culture and inhibited the generation of progenitor cells capable of forming small eosinophil colonies or clusters in soft agar cultures. The results of these in vivo experiments directly show that IL-5 is an essential regulatory molecule required for the bone marrow-dependent phase of a parasite-induced eosinophilia.
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Hall, Laurie R., Jussuf T. Kaifi, Eugenia Diaconu, and Eric Pearlman. "CD4+ Depletion Selectively Inhibits Eosinophil Recruitment to the Cornea and Abrogates Onchocerca volvulus Keratitis (River Blindness)." Infection and Immunity 68, no. 9 (September 1, 2000): 5459–61. http://dx.doi.org/10.1128/iai.68.9.5459-5461.2000.
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ABSTRACT Previous studies demonstrated that in the murine model ofOnchocerca volvulus keratitis, neutrophils and eosinophils are recruited into the cornea in a biphasic manner in response to intrastromal injection. To determine if CD4+ T cells regulate migration of neutrophils and eosinophils into the cornea, CD4+ cells were depleted using monoclonal antibody GK1.5 before intrastromal injection of parasite antigens. Depletion of CD4+ cells abrogated corneal opacification at later but not early stages of disease. Consistent with this observation, CD4 depletion significantly impaired recruitment of eosinophils to the cornea but had no effect on neutrophils. These data indicate that CD4+ T cells mediate sustained O. volvuluskeratitis by regulating eosinophil recruitment to the cornea.
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Daly, Christine M., Graham Mayrhofer, and Lindsay A. Dent. "Trapping and Immobilization ofNippostrongylus brasiliensis Larvae at the Site of Inoculation in Primary Infections of Interleukin-5 Transgenic Mice." Infection and Immunity 67, no. 10 (October 1, 1999): 5315–23. http://dx.doi.org/10.1128/iai.67.10.5315-5323.1999.
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ABSTRACT Interleukin-5 (IL-5) transgenic mice are highly resistant to primary infections with the intestinal nematode Nippostrongylus brasiliensis; few parasites are found in the intestines of infected animals, and egg production is minimal. While adult worms may be damaged in the intestine, larval migration, development, and viability may also be impaired in other tissues. This study addresses the migration of N. brasiliensis larvae through the skin and lungs and associated cellular responses in primary infections of IL-5 transgenic mice. Although some larvae may have been trapped and killed in the lungs of IL-5 transgenic mice, most apparently failed to reach this site. Two or more hours after infection of IL-5 transgenic mice, eosinophils were a major component of the cellular infiltrate at the subcutaneous site of injection, and localized eosinophil degranulation was extensive. Seventy-five to ninety-five percent of the larvae injected into subcutaneous air pouches in IL-5 transgenic mice were retained there for at least 24 h. In contrast, in nontransgenic mice, less than 20% of larvae could be recovered from the skin 2 or more h postinjection, and eosinophil activity was modest at all times. The data strongly suggest that eosinophils can restrict the movement of N. brasiliensis larvae in the first few hours of a primary infection and that this has profound effects on later stages of parasite development. Preexisting eosinophilia, due either to allergy or to infection with tissue-invasive helminth species, may therefore confer some degree of immediate and nonspecific resistance in primary infections with parasitic worms.
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Kaneko, M., S. Horie, M. Kato, G. J. Gleich, and H. Kita. "A crucial role for beta 2 integrin in the activation of eosinophils stimulated by IgG." Journal of Immunology 155, no. 5 (September 1, 1995): 2631–41. http://dx.doi.org/10.4049/jimmunol.155.5.2631.
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Abstract An IgG-coated surface, such as found on parasites, is one of the most effective physiologic stimuli for eosinophil activation. Recent evidence suggests that cellular adhesion, especially that through the beta 2 integrin, is an important step in cellular activation and accumulation. Therefore, we investigated the role of adhesion molecules in IgG-stimulated eosinophil functions. Cross-linking of eosinophil cytophilic IgG by anti-IgG immobilized to tissue culture plates induced degranulation, whereas soluble anti-IgG did not. Similarly, eosinophils exposed to human IgG immobilized to plates adhered and degranulated; in addition, adherence and subsequent degranulation were inhibited by mAbs to CD18 and CD11b, but not by mAb to CD29, suggesting an important role of beta 2 integrin for these responses. Eosinophil degranulation induced by IgG covalently coupled to Sepharose 4B beads was also inhibited by mAb to CD18. Furthermore, fibrinogen, a ligand for CD11b/18, showed synergistic enhancement of IgG-induced degranulation when it was co-immobilized with IgG to plates. A morphologic study showed that eosinophils, stimulated by immobilized IgG, protrude numerous pseudopods; this morphologic change was inhibited by mAb to CD18. This cellular adhesion seems to affect the early signaling events in eosinophils because the production of inositol phosphates was abolished by mAb to CD18. Interestingly, although superoxide production by eosinophils triggered by immobilized IgG was inhibited by mAb to CD18, superoxide production and morphologic change of neutrophils were not. These results suggest that cell adhesion through CD11b/18 is a crucial step for the activation, signaling, and effector function of eosinophils stimulated by IgG.
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Darlan, Dewi Masyithah, Zaimah Z. Tala, Cellya Amanta, Syah Mirsya Warli, and Nurfida Khairina Arrasyid. "Correlation between Soil Transmitted Helminth Infection and Eosinophil Levels among Primary School Children in Medan." Open Access Macedonian Journal of Medical Sciences 5, no. 2 (February 22, 2017): 142–46. http://dx.doi.org/10.3889/oamjms.2017.014.
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BACKGROUND: Soil Transmitted Helminth infection is one of most prevalent health problems worldwide, especially in environments with poor sanitation. Based on World Health Organisation (WHO) data, more than 2 billion people, or 24% of the world's population, are infected with intestinal parasite. The highest prevalence is located in areas of poor sanitation and unsafe water supplies. In Indonesia, the prevalence of parasite infections is 15% of the entire population.AIM: The purpose of this study was to determine the relationship between Soil Transmitted Helminth infection on levels of eosinophils among primary school children. In addition, this study also aimed to determine the prevalence of different types of worm infections and the levels of eosinophils in children infected with worms.MATERIAL AND METHODS: This study was analytic observational using a cross-sectional method. The sampling technique was consecutive and in total 132 samples was obtained. The study involved primary school children in Amplas Medan and Hamparan Perak, Deli Serdang through May to October 2016. Univariate analysis was performed to determine STH infection prevalence and bivariate analysis was used to find the correlation between STH infection and eosinophil levels through a Chi square (X2) test. RESULTS: The results showed that the prevalence of Soil Transmitted Helminth was 7.6%. The most common types of STH infection were 3.8% with Trichuris trichiura and 3% with Ascaris lumbricoides. A significant correlation was found between Parasite infection and eosinophil levels (Contingency Coefficient (C) = 0.2, X2 = 5.3, p = 0.021) and the risk of STH infection that caused eosinophilia or increased eosinophil levels in the children with a Prevalence Ratio (PR) of 1.56 (Confidence Interval (CI) 95%: 1.10-2.22).CONCLUSION: It is recommended that schools at similar risk improve and maintain hygiene and healthy behaviour in the school environment and that parents and teachers pay greater attention to the cleanliness of their children.
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Hansen, Rowena D. E., Alexander J. Trees, Germanus S. Bah, Udo Hetzel, Coralie Martin, Odile Bain, Vincent N. Tanya, and Benjamin L. Makepeace. "A worm's best friend: recruitment of neutrophils by Wolbachia confounds eosinophil degranulation against the filarial nematode Onchocerca ochengi." Proceedings of the Royal Society B: Biological Sciences 278, no. 1716 (December 22, 2010): 2293–302. http://dx.doi.org/10.1098/rspb.2010.2367.
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Onchocerca ochengi , a filarial parasite of cattle, represents the closest relative of the human pathogen, Onchocerca volvulus . Both species harbour Wolbachia endosymbionts and are remarkable in that adult female worms remain viable but sessile for many years while surrounded by host cells and antibodies. The basis of the symbiosis between filariae and Wolbachia is thought to be metabolic, although a role for Wolbachia in immune evasion has received little attention. Neutrophils are attracted to Wolbachia , but following antibiotic chemotherapy they are replaced by eosinophils that degranulate on the worm cuticle. However, it is unclear whether the eosinophils are involved in parasite killing or if they are attracted secondarily to dying worms. In this study, cattle infected with Onchocerca ochengi received adulticidal regimens of oxytetracycline or melarsomine. In contrast to oxytetracycline, melarsomine did not directly affect Wolbachia viability. Eosinophil degranulation increased significantly only in the oxytetracycline group; whereas nodular gene expression of bovine neutrophilic chemokines was lowest in this group. Moreover, intense eosinophil degranulation was initially associated with worm vitality, not degeneration. Taken together, these data offer strong support for the hypothesis that Wolbachia confers longevity on O. ochengi through a defensive mutualism, which diverts a potentially lethal effector cell response.
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Schollaert, Kaila L., Melissa K. Mingler, Marc E. Rothenberg, and Patricia C. Fulkerson. "Negative Regulation of Eosinophil Production by Toll-Like Receptors." Blood 120, no. 21 (November 16, 2012): 1237. http://dx.doi.org/10.1182/blood.v120.21.1237.1237.
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Abstract Abstract 1237 Eosinophilia is a common clinical problem associated with numerous disorders such as atopic diseases, parasitic infections, hypereosinophilic syndrome (HES), and cancer. A marked decrease in circulating eosinophils, or eosinopenia, has long been associated with acute bacterial infections. Eosinopenia has been shown to be a sensitive and reliable marker for distinguishing between non-infectious and infection-associated sepsis in the intensive care unit setting. Eosinopenia with acute infection had been assumed to be secondary to the release of adrenal glucocorticoids in response to the stress of infection. However, animal studies performed in the 1970s demonstrated that inhibition of parasite-associated eosinophilia with acute bacterial infection was independent of adrenal stimulation; the investigator speculated that it was due to a direct effect on the eosinophil precursor. To date, the mechanism of infection-associated eosinopenia, and its potential for suppressing IL-5-mediated eosinophilia, has not been investigated. To study eosinophil development, we established an ex vivo liquid culture system in which we can follow the differentiation of murine eosinophil lineage-committed progenitors (EoPs) to mature functional effector eosinophils that express known eosinophil surface markers and granule proteins and respond to eosinophil-active chemoattractants. We demonstrate that murine eosinophil precursors express mRNA for six TLRs. Ligands for TLR2 heterodimers, TLR4 and TLR7, but not TLR3, inhibited eosinophil ex vivo growth by attenuating EoP proliferation in response to IL-5 stimulation. Exposure to heat-killed E. coli also resulted in diminished EoP proliferation. The developing eosinophils further responded to TLR activation with production of a subset of inflammatory cytokines, including IL-6, IL-10, TNF-alpha and CXCL10. Co-culturing of untreated EoPs with LPS-exposed EoPs resulted in reduced IL-5-mediated proliferation of the untreated EoPs, suggesting that EoPs secrete mediators in response to TLR activation that regulate their proliferation in an autocrine/paracrine manner. Neutralization of IFN-beta, but not IFN-alpha or IFN-gamma, partially protected developing eosinophils from the inhibitory effects of LPS. In vivo studies revealed that endotoxemia and bacteremia reduced numbers of EoPs in the bone marrow of wild-type mice. Further, LPS dose-dependently reduced hypereosinophilia in IL-5 transgenic mice, highlighting the potential therapeutic value of this approach even in an extreme IL-5-driven clinical state. Suppression of eosinophil production by TLR4 ligands is conserved between mice and humans as yield of eosinophils from human EoPs was reduced following LPS exposure. Taken together, these findings identify a mechanistic explanation for eosinopenia following bacterial infections and identify a novel therapeutic strategy for inhibiting eosinophil production and peripheral eosinophilia in eosinophil-associated diseases. Disclosures: No relevant conflicts of interest to declare.
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Shin, Myeong Heon, Hirohito Kita, Hae Young Park, and Ju Young Seoh. "Cysteine Protease Secreted by Paragonimus westermani Attenuates Effector Functions of Human Eosinophils Stimulated with Immunoglobulin G." Infection and Immunity 69, no. 3 (March 1, 2001): 1599–604. http://dx.doi.org/10.1128/iai.69.3.1599-1604.2001.
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ABSTRACT An immunoglobulin G (IgG)-coated surface, such as that found on helminth parasites, is one of the most effective physiologic stimuli for eosinophil activation. The cysteine proteases secreted by tissue-invasive helminth larvae play an important role in evasion of the immune response by degrading the host immunoglobulins. In this study, we investigated whether cysteine proteases in the excretory-secretory product (ESP) produced by Paragonimus westermani newly excysted metacercariae (PwNEM), which cause pulmonary or extrapulmonary paragonimiasis in human beings, could modify effector functions of human eosinophils stimulated with IgG. We coated 96-well plates with human IgG in the absence or presence of the ESP produced by PwNEM. When eosinophils were incubated in the wells coated with IgG in the presence of the ESP, eosinophil degranulation and superoxide production were significantly reduced compared with results for cells incubated in wells coated with IgG alone. This inhibitory effect of the ESP on IgG-induced superoxide production was dose dependent and was significantly abolished by pretreatment of the ESP with heat. These findings suggest that the cysteine proteases secreted by PwNEM attenuate both activation and degranulation of eosinophils stimulated with IgG. Thus, the cysteine proteases produced by tissue-invasive helminth larvae play crucial roles in evasion of IgG-dependent eosinophil helminthotoxicity and in reduction of eosinophil-associated tissue inflammation during the migratory period.
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Mawhorter, S. D., D. A. Stephany, E. A. Ottesen, and T. B. Nutman. "Identification of surface molecules associated with physiologic activation of eosinophils. Application of whole-blood flow cytometry to eosinophils." Journal of Immunology 156, no. 12 (June 15, 1996): 4851–58. http://dx.doi.org/10.4049/jimmunol.156.12.4851.
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Abstract Activation is central to the eosinophil's functional role as an immune responder cell. To evaluate such activation in cells freshly isolated from peripheral blood, a method for whole-blood immunostaining and flow cytometry-based eosinophil selection was developed. Simultaneous comparison of purified eosinophils and whole-blood cells revealed significant differences in the levels of expression of various surface molecules, which suggested that the purification process activated the eosinophils. Subsequent analyses were conducted with the whole-blood assay. When eosinophils from helminth-infected persons (n = 18) were compared with those from normal individuals (n = 10), the early activation marker CD69 was found to be significantly increased (geometric mean (GM) = 4.3 vs. 1.0%, p = 0.04). The granulocyte activation marker CD66 was also up-regulated on eosinphils from helminth patients (GM = 53.3 vs. 31.0%, p = 0.044), as was the tetraspan family molecule CD81 (TAPA-1; GM = 79.4 vs. 48.2%, p = 0.02). Conversely, in vivo CD23 (FcepsilonRII) expression on eosinophils was decreased in the presence of parasitic infection (GM = 0.9 vs. 5.7%, p = 0.02). Expression of the eosinophil surface molecules CD69, CD81, and CD23 was significantly enhanced after cytokine stimulation in vitro with IL-3 or GM-CSF. In vivo, specific anthelmintic therapy resulted in decreased CD66 and CD25 expression (p < 0.05 compared with pretreatment) to levels approaching those seen in uninfected normal individuals. These findings indicate the dynamic nature of eosinophil surface molecules and demonstrate an important role for whole-blood staining in developing an understanding of the nature of eosinophil activation and of their role in inflammatory reactions to helminth parasites.
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Muturi, K. N., M. Wallace, J. Struthers, J. R. Scaife, M. A. Lomax, A. Mackellar, J. F. Huntley, and R. L. Coop. "The influence of n-6 and n-3 polyunsaturated fatty acids on eosinophils numbers in the gut of milk or milk replacer fed calf." Proceedings of the British Society of Animal Science 2003 (2003): 86. http://dx.doi.org/10.1017/s175275620001245x.
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Infection by parasites is a major cause of production losses and mortality in young calves. The problem is most prevalent during the first grazing season (Armour, 1989). Eosinophils are important cellular mediators in immunity to gastrointestinal parasites (Baker et al, 1993), but during an extreme hypersensitivity immune response, degranulating eosinophils may lead to tissue pathology which may favour parasite survival (Miller, 1996). Dietary polyunsaturated fatty acids (PUFA) influence the fatty acid composition of immune tissues and cells (Jaffrey, 1998). n-6 and n-3 fatty acids are known to influence various components of immune response via eicosanoid dependent or independent mechanisms which influence the relative proportions of Th1 and Th2 cytokines, including IL-5 an important regulator of eosinophils maturation and recruitment. This study was carried out to establish the extent to which dietary n-6 or n-3 PUFA source affects the numbers of eosinophils in the gut of calves.
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Sanderson, C. J., D. J. Warren, and M. Strath. "Identification of a lymphokine that stimulates eosinophil differentiation in vitro. Its relationship to interleukin 3, and functional properties of eosinophils produced in cultures." Journal of Experimental Medicine 162, no. 1 (July 1, 1985): 60–74. http://dx.doi.org/10.1084/jem.162.1.60.
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Factors stimulating eosinophil differentiation in vitro have been studied by means of a liquid bone marrow culture system in which the number of eosinophils is estimated directly by morphology or indirectly by assay for eosinophil peroxidase. The results show that eosinophil colonies are not formed in agar, emphasizing the importance of the liquid culture system. Three types of evidence identify a novel lymphokine, eosinophil-differentiating factor (EDF). (a) Coordinate analysis of lymphokine activity in media conditioned by a panel of parasite antigen and another panel of alloantigen-reactive T cell clones indicates that EDF is distinct from interleukin 2 (IL-2), IL-3, and bone marrow proliferation activity (BMPA). (b) A T hybrid (NIMP-TH1) produces EDF but no IL-2, IL-3, interferon, or colony-stimulating factor. (c) Gel filtration of conditioned media (CM) indicates that NIMP-TH1 and a T clone (NIMP-T2) produce EDF (Mr 46,000). NIMP-T2 also produced IL-3 (Mr 26,000) but this was easily separated from EDF. IL-3 is also shown to have eosinophil differentiation activity (EDA) but this represents a very small proportion of the EDA in T2-CM. Fractionation of WEHI-3-CM indicates that EDA from this source has a similar elution profile to IL-3 (Mr 35-36,000). Furthermore, a comparison of the relative activities in purified IL-3 and WEHI-3-CM indicates that all the EDA can be attributed to the IL-3 in the latter. EDF is shown to stimulate production of eosinophils in long-term bone marrow cultures; the kinetics of eosinophil production suggests that EDF is acting on committed precursors in the bone marrow. The transient nature of eosinophil production suggests that precursors from multipotential stem cells are not produced. The eosinophils produced in these cultures are morphologically normal and functional in that they lysed sheep red blood cells coated with IgG1, IgG2a, and IgG2b, but not with IgM, IgA, or IgE. In addition, they were capable of adhering to and killing Schistosoma mansoni schistosomula.
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Olsson, Andre, Nathan Salomonis, Harinder Singh, and H. Leighton Grimes. "Identification of the Origin of Eosinophils." Blood 126, no. 23 (December 3, 2015): 886. http://dx.doi.org/10.1182/blood.v126.23.886.886.
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Abstract Eosinophil granulocytes participate in parasite protection and also play a part in asthma and allergy. Histology staining shows a characteristic red granular stain, which separates the eosinophils from neutrophil and basophil granulocytes. Eosinophils can be characterized by SiglecF and CCL3 surface expression, and differentiate from bone-marrow CD34+ Granulocyte Monocyte Progenitors (GMP). Isolating GMP and stimulating with IL-3, GM-CSF and IL-5 leads to eosinophil colony forming units (CFU) in methylcellulose. Eosinophil precursors are currently are isolated by IL-5ra expression in GMP and IL-5 is critical for eosinophil differentiation and expansion both in vivo and in vitro. Gata1 is a transcription factor necessary for erythrocyte and megakaryocyte formation. Previously, a Gata1-GFP transgenic reporter mouse was used to show that all eosinophil CFU capacity within the GMP came from those cells which induce Gata1 expression. Apart from that, little is known about the required transcriptional activity for eosinophil development. We performed single cell RNA seq using the Fluidigm C1 system on murine hematopoietic stem and progenitor cells to characterize myeloid differentiation and development. While primarily studying neutrophil granulocyte differentiation programs within the GMP, we noticed progenitors that expressed eosinophil genes. Gfi1 is a known granulocyte transcription factor, which is critical for neutrophil granulocytes in mice and man. We utilized a Gfi1-GFP knock in reporter mouse to exclude Gfi1-GFPhigh GMP (which we find are neutrophil precursors). Unbiased hierarchical clustering of single-cell RNA Seq from Gfi1-GFPlow GMP identified four clusters. To identify uniquely expressed transcripts within each cluster, we utilized the MarkerFinder algorithm in a bioinformatics analysis platform called AltAnalyze (p<0.05 and fold >2). One cluster expressed transcripts like Fos, Jun, Gata1 and Gata2, indicating a stem-like progenitor. A second cluster, lost the stem-progenitor signature but expressed Elane, Mpo and Csf3r, suggesting a neutrophil progenitor signature. A third cluster lost Fos and Jun expression while gaining Il5ra, Epx and Prg2, suggesting that this cluster contained eosinophil-primed progenitors. Interestingly, although part of the stem-progenitor gene expression was lost, this cluster retained Gata1 expression. Thus, we have identified rare Gata1-expressing GMP populations with either a stem-progenitor or an eosinophil gene expression program. To biologically test whether Gfi1-GFPlow GMP have eosinophil potential, we performed CFU assays with or without IL-5 and then analyzed the colonies for eosinophil markers. We found that IL-5 stimulation of Gfi1-GFPlow GMP led to a significant CFU-G eosinophil-like colony formation, whereas IL-5 stimulation of Gfi1-GFPhigh GMP did not result in any eosinophil-like colonies. Flow cytometric analysis showed SiglecF and CCL3 surface expression in IL-5 treated Gfi1-GFPlow GMP. Furthermore, we observed increased IL-5ra, Epx and Prg2 transcript levels in IL-5 treated Gfi1-GFPlow GMP. Histology stain showed characteristic eosinophilic granules in the IL-5 treated condition. While earlier studies posited the induction of Gata1 expression in GMP as part of the program leading to eosinophil development, our data reveal a rare Gata1-expressing stem-progenitor population which gives rise to eosinophil progenitors as these cells differentiate along the granulocyte-monocyte pathway. Thus, single-cell RNA Seq, combined with conventional methodology can be used to define previously rare and intermediary progenitor populations to understand hematopoietic development. Disclosures No relevant conflicts of interest to declare.
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Morassutti, Alessandra L., and Carlos Graeff-Teixeira. "Interface Molecules ofAngiostrongylus cantonensis: Their Role in Parasite Survival and Modulation of Host Defenses." International Journal of Inflammation 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/512097.
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Angiostrongylus cantonensisis a nematode parasite that causes eosinophilic meningoencephalitis in humans. Disease presents following the ingestion of third-stage larvae residing in the intermediate mollusk host and disease manifests as an acute inflammation of the meninges characterized by eosinophil infiltrates which release a battery of proinflammatory and cytotoxic agents in response to the pathogen. As a mechanism of neutralizing these host defenses,A. cantonensisexpresses different molecules with immunomodulatory properties that are excreted or secreted (ES). In this paper we discuss the role of ES proteins on disease exacerbation and their potential use as therapeutic targets.
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Santos, Jairo Ivo dos, and Cidônia de Lourdes Vituri. "Some hematimetric findings in human Giardia lambia infection." Revista do Instituto de Medicina Tropical de São Paulo 38, no. 2 (April 1996): 91–95. http://dx.doi.org/10.1590/s0036-46651996000200002.
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Up to now few reports about haematological alterations induced by Giardia lamblia infection have been described. Because there are questions on this matter still not answered, we carried out a study to evaluate some erythrometric and leucometric parameters in a sample that consisted of 55 patients exclusively infected with G. lamblia and of 55 sex and age matched parasite-free individuals. The haematological parameters evaluated were: mean corpuscular volume (MCV), hemoglobin concentration, and relative and absolute number of eosinophils and lymphocytes. No significant differences in the mean values of MCV, hemoglobin levels and absolute relative lymphocyte numbers between the two groups could be detected. When the giardiasis and control groups were separated by pediatric (0-18 years old) and adult (older than 18 years) classes, a very significant difference in both relative and absolute number of eosinophils in the adult class was observed. With respect of the pediatric class, no differences, either in relative and absolute number of eosinophils, could be observed. Our findings suggest that, during G. lamblia infection, some kind of parasite allergen(s) could be secreted and be responsible for the increasing of eosinophil counts in peripheral blood of adults.
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Grangette, C., V. Gruart, M. A. Ouaissi, F. Rizvi, G. Delespesse, A. Capron, and M. Capron. "IgE receptor on human eosinophils (FcERII). Comparison with B cell CD23 and association with an adhesion molecule." Journal of Immunology 143, no. 11 (December 1, 1989): 3580–88. http://dx.doi.org/10.4049/jimmunol.143.11.3580.
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Abstract IgE FcR (FcERII) on human eosinophils was characterized and compared with FcERII present on B cells (CD23). Two mAb, BB10 (anti-eosinophil FcERII) and 135 (anti-CD23), bound to the major component of FcERII at 45,000 to 50,000 Mr, both on purified hypodense eosinophils and on a B cell line (WIL-2WT). The specific ligand, human myeloma IgE, was able to bind to the molecules immunoprecipitated by BB10. A cross-reactivity between BB10 and a mAb anti-Leishmania gp63, which is a "fibronectin (Fn)-like" molecule, containing the L-arginine-L-glycyl-L-aspartyl (RGD) cell attachment domain indicated the presence of such a sequence in the common structure present on eosinophil and B cell FcERII. The synthetic tetrapeptide RGDS as well as its inverted sequence (SDGR) reduced the binding of BB10 and anti-Fn mAb to eosinophils and B cells. Flow microfluorometry analysis revealed a variable binding of BB10 and anti-Fn mAb to eosinophils purified from different patients, results compatible with recent findings on the inducibility of FcERIIb. The significant inhibition of IgE-dependent cytotoxicity against parasite targets by preincubation of eosinophils with BB10, anti-Fn and anti-CD23 mAb, with anti-RGDS polyclonal antibodies or with the SDGR peptide suggested the requirement of this cell adhesion sequence for the function of low affinity FcERII. The presence of such a sequence in the C-terminal domain of B cell FcERII raised the possibility of its role in B cell adhesion or B cell growth.
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Molofsky, Ari B., Jesse C. Nussbaum, Hong-Erh Liang, Steven J. Van Dyken, Laurence E. Cheng, Alexander Mohapatra, Ajay Chawla, and Richard M. Locksley. "Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages." Journal of Experimental Medicine 210, no. 3 (February 18, 2013): 535–49. http://dx.doi.org/10.1084/jem.20121964.
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Eosinophils in visceral adipose tissue (VAT) have been implicated in metabolic homeostasis and the maintenance of alternatively activated macrophages (AAMs). The absence of eosinophils can lead to adiposity and systemic insulin resistance in experimental animals, but what maintains eosinophils in adipose tissue is unknown. We show that interleukin-5 (IL-5) deficiency profoundly impairs VAT eosinophil accumulation and results in increased adiposity and insulin resistance when animals are placed on a high-fat diet. Innate lymphoid type 2 cells (ILC2s) are resident in VAT and are the major source of IL-5 and IL-13, which promote the accumulation of eosinophils and AAM. Deletion of ILC2s causes significant reductions in VAT eosinophils and AAMs, and also impairs the expansion of VAT eosinophils after infection with Nippostrongylus brasiliensis, an intestinal parasite associated with increased adipose ILC2 cytokine production and enhanced insulin sensitivity. Further, IL-33, a cytokine previously shown to promote cytokine production by ILC2s, leads to rapid ILC2-dependent increases in VAT eosinophils and AAMs. Thus, ILC2s are resident in VAT and promote eosinophils and AAM implicated in metabolic homeostasis, and this axis is enhanced during Th2-associated immune stimulation.
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Ridel, P. R., C. Auriault, F. Darcy, R. J. Pierce, P. Leite, F. Santoro, J. L. Neyrinck, J. P. Kusnierz, and A. Capron. "Protective role of IgE in immunocompromised rat toxoplasmosis." Journal of Immunology 141, no. 3 (August 1, 1988): 978–83. http://dx.doi.org/10.4049/jimmunol.141.3.978.
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Abstract In contrast to euthymic adult Fischer rats, immunocompromised Nu/Nu animals develop a lethal infection when inoculated with the RH strain of the protozoan Toxoplasma gondii. However, a significant period of survival is obtained when Nu/Nu rats are passively transferred with sera from 28-day infected Fischer +/+ (euthymic) animals. Specific IgE are involved since IgE-depleted sera are unable to afford such a protection. Only excreted/secreted Ag or living tachyzoites are able to induce a significant protective IgE response in intact animals. In addition, platelets or, to a lesser extent, eosinophil-rich populations from Toxoplasma infected or excreted-secreted Ag-immunized euthymic animals bear surface IgE and are cytotoxic for the parasite in vitro. Also, adoptive transfer of immune platelets confers a significant degree of protection to Toxoplasma-infected Nu/Nu animals. Our results clearly show the key role of Ag present in both living parasites and excreted-secreted Ag to induce, in this model, a protective IgE response. In addition, as in other parasitic infections, platelets and probably eosinophils are the effector cells involved in controlling parasitic dissemination during Toxoplasma infection in immunocompromised rats.
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Hashimoto, Takashi, Kanako Muneta, and Ken Watanabe. "Facial Edema in an Elderly Man: An Unusual Presentation of Nonepisodic Angioedema with Eosinophilia." Case Reports in Dermatology 9, no. 3 (September 12, 2017): 164–68. http://dx.doi.org/10.1159/000480398.
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Nonepisodic angioedema with eosinophilia (NEAE) is a rare allergic disease with a young Japanese and East Asian female predominance. NEAE features transient, nonrecurrent angioedema and peripheral blood eosinophilia without visceral organ involvement. Angioedema in NEAE occurs on the extremities, while the trunk and face are rarely involved. Here, we report a case of NEAE affecting only the face in an 80-year-old Japanese man. He was otherwise healthy and took no medication until the sudden development of angioedema on the face. The extremities and trunk were not involved. Skin biopsy examination revealed eosinophilic infiltration and degranulation between collagen bundles through the entire dermis, and perivascular and perifollicular infiltration of eosinophils and lymphocytes, but no evidence of vasculitis. Peripheral hypereosinophilia and high serum thymus- and activation-regulated chemokine (TARC) level were noted. Visceral organ involvement, parasite infection, and an allergic response were not detected in the patient. Administration of oral corticosteroid improved his symptoms rapidly and dramatically with improvements in the blood eosinophil count and serum TARC level. After the corticosteroid was discontinued, no recurrence was observed for 3 years. Thus, he was diagnosed as having NEAE. It should be noted that angioedema with eosinophilia might occur with an unusual presentation and might develop in elderly patients.
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Bansal, Sharad, Mukesh Gupta, Deepak Sharma, and Shweta Bansal. "A Rare Case of Ibuprofen-Induced Eosinophilic Meningitis in a 13-Year-Old Girl." Clinical Medicine Insights: Pediatrics 8 (January 2014): CMPed.S13829. http://dx.doi.org/10.4137/cmped.s13829.
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Eosinophilic meningoencephalitis is based on clinical manifestations and microscopic identification of eosinophils present in cerebrospinal fluid (CSF). It is caused by a variety of helminthic infections with most common being angiostrongyliasis, gnathostomiasis, toxocariasis, cysticercosis, schistosomiasis, baylisascariasis, and paragonimiasis. Many case reports are there in which parasites have been found responsible, but there are rare reports of CSF eosinophilia associated with the use of drugs. We report a case of drug-induced (ibuprofen) eosinophilic meningitis in a healthy female who presented to us with severe headache and improved dramatically after drug withdrawal.
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Phuyal, S., V. C. Jha, and M. Subedi. "Prevalence of Blood Parasites in Dogs of Kathmandu Valley." Nepalese Veterinary Journal 34 (December 21, 2017): 107–12. http://dx.doi.org/10.3126/nvj.v34i0.22909.
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Study in blood parasitic diseases in dog was carried out from August 2014 to November 2014 to find out the prevalence of haemoparasites in clinical cases of hyperthermia in dogs. Blood sample from 50 cases of hyperthermia were collected and examined for any blood parasites by the smear method. The haematological parameter (RBC, WBC, PCV, Hb, & DLC) of each sample was also assessed and analyzed. Data was analyzed to determine prevalence of various species of blood parasites to establish the correlation of the infections with age, sex and breed. Out of 50 samples examined, blood parasites were determined in 12 percent samples of which 2(4%) were positive for Babesia canis and 4 (8%) were positive for Ehrlichia spp. The percentage of infection was greater in female 4(16.67%) than male 2(7.14%). The prevalence of blood parasite was higher in German shepherd. The prevalence of blood parasite was higher in 2-4 years of dogs. To determine significant difference between the hematological parameter of infected and non-infected cases, t-test was need (R, version 3.0.3). The confidence level for the analysis was set at 95percent with significance level assessed at p< 0.05. The study between the infected and non-infected host revealed statistically significant difference in PCV, Neutrophil and Eosinophil. Whereas other parameters did not have any significant difference. The mean PCV was significantly low (P <0.05) in infected dog than in non-infected dog. Mean Neutrophil was significantly decreased whereas Eosinophil was increased in infected dogs than in non-infected dogs.