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1
Varlamov, E. E., T. V. Vinogradova, A. A. Chuslyaeva, T. S. Okuneva e A. N. Pampura. "BIOMARKERS ALLERGIC INFLAMATION AND SEVERITY OF ATOPIC DERMATITIS AT CHILDREN". Russian Journal of Allergy 9, n. 5 (15 dicembre 2012): 31–35. http://dx.doi.org/10.36691/rja694.
Testo completoAbstract (sommario):
Background.To establish the relationship between the serum concentrations of IL4, IL5, eotaxin, eotaxin2, ECP and the severity of atopic dermatitis in children. Methods. The study included 40 children with atopic dermatitis, patients were divided into two clusters with KMeans method, index SCORAD was taken as a criterion of clustering. All patients were conducted to determine the concentration of IL4, IL5, eotaxin, eotaxin2, ECP. Results. The SCORAD index was significantly higher in the second cluster in comparison to the first one. In second cluster the level of eotaxin2 was significantly higher, in terms of the ECP, IL4, IL5,eotaxin patient groups did not differ. The second cluster was characterized by patients with a concentration of IL5 of 1,5 p/ml. Conclusion. In assessing the severity of allergic inflammation in atopic dermatitis concentration of eotaxin2 was most informative.
2
Badewa, A. P., C. E. Hudson e A. S. Heiman. "Regulatory Effects of Eotaxin, Eotaxin-2, and Eotaxin-3 on Eosinophil Degranulation and Superoxide Anion Generation1". Experimental Biology and Medicine 227, n. 8 (settembre 2002): 645–51. http://dx.doi.org/10.1177/153537020222700814.
Testo completoAbstract (sommario):
Eosinophilic leukocytes have been implicated as primary effector cells in inflammatory and allergic diseases. When activated by cytokines, human eosinophils secrete and produce a variety of proinflammatory or tissue damaging substances. Although well known for their chemoattractant effects, little is known about the precise contribution of the eosinophil-selective chemokines, eotaxin, eotaxin-2, and eotaxin-3 to the effector functions of eosinophils. This forms the central focus of these investigations for which clone 15-HL-60 human eosinophilic cells were used as the in vitro model. Investigation results suggest that all three subtypes of eotaxin directly stimulate eosinophil superoxide anion generation that is inhibited by neutralizing eotaxin antibody or pretreatment of cells with the receptor antibody anti-CCR3. Pretreatment or co-treatment with each of the eotaxins augmented phorbol myristate-induced superoxide generation. Concentration-dependent degranulation of eosinophil peroxidase was noted for all three chemokines, and potentiation of calcium lonophore-induced degranulation was observed with eotaxin pretreatments. Results of interleukin-5 pretreatment studies suggest that the eotaxin chemokines may act cooperatively to enhance effector functions of eosinophils. Collectively, the present studies have advanced knowledge of the eotaxin family of chemokines to include eosinophil priming and modulation of eosinophil activation and secretion effector functions.
3
Haley, Kathleen J., Mary E. Sunday, Yolanda Porrata, Colleen Kelley, Anne Twomey, Aliakbar Shahsafaei, Benjamin Galper, Larry A. Sonna e Craig M. Lilly. "Ontogeny of the eotaxins in human lung". American Journal of Physiology-Lung Cellular and Molecular Physiology 294, n. 2 (febbraio 2008): L214—L224. http://dx.doi.org/10.1152/ajplung.00086.2007.
Testo completoAbstract (sommario):
The ontogeny of the C-C chemokines eotaxin-1, eotaxin-2, and eotaxin-3 has not been fully elucidated in human lung. We explored a possible role for eotaxin in developing lung by determining the ontogeny of eotaxin-1 (CCL11), eotaxin-2 (CCL24), eotaxin-3 (CCL26), and the eotaxin receptor, CCR3. We tested discarded surgical samples of developing human lung tissue using quantitative RT-PCR (QRT-PCR) and immunostaining for expression of CCL11, CCL24, CCL26, and CCR3. We assessed possible functionality of the eotaxin-CCR3 system by treating lung explant cultures with exogenous CCL11 and analyzing the cultures for evidence of changes in proliferation and activation of ERK1/2, a signaling pathway associated with CCR3. QRT-PCR analyses of 22 developing lung tissue samples with gestational ages 10–23 wk demonstrated that eotaxin-1 mRNA is most abundant in developing lung, whereas mRNAs for eotaxin-2 and eotaxin-3 are minimally detectable. CCL11 mRNA levels correlated with gestational age ( P < 0.05), and immunoreactivity was localized predominantly to airway epithelial cells. QRT-PCR analysis detected CCR3 expression in 16 of 19 developing lung samples. Supporting functional capacity in the immature lung, CCL11 treatment of lung explant cultures resulted in significantly increased ( P < 0.05) cell proliferation and activation of the ERK signaling pathway, which is downstream from CCR3, suggesting that proliferation was due to activation of CCR3 receptors by CCL11. We conclude that developing lung expresses the eotaxins and functional CCR3 receptor. CCL11 may promote airway epithelial proliferation in the developing lung.
4
Varlamov, E. E., O. G. Elisyutina, T. V. Vinogradova, E. S. Fedenko e A. N. Pampura. "AGE-RELATED PATHOGENTIC SPECIFICITY OF CYTOKINE PROFILE IN ATOPIC DERMATITIS PATIENTS". Russian Journal of Allergy 13, n. 4-5 (15 dicembre 2016): 37–42. http://dx.doi.org/10.36691/rja358.
Testo completoAbstract (sommario):
Background. In this article the results of own research of the cytokine profile in atopic dermatitis (AD) adults and children depending on age are provided. Materials and methods. 88 patients with AD (54 children aged from 1 year to 16 years old and 24 adults aged from 21 years to 56 years old) were included in the study. Cytokine profile of a number of cytokines: IL-4, IL-5, IL-22, IL-31, IL-33, and transforming growth factor TGFβ1, eotaxin, eotaxin2 was examined. Results. Significant differences in IL-22, CC chemokines (eotaxin and eotaxin-2) and TGFβ levels depending on the age and severity of atopic dermatitis were found.
5
Diny, Nicola, Xuezhou Hou, Jobert G. Barin, Monica V. Talor, Noel R. Rose e Daniela Cihakova. "The eotaxin-CCR3 pathway is required for eosinophil trafficking to the heart in eosinophilic myocarditis". Journal of Immunology 196, n. 1_Supplement (1 maggio 2016): 117.10. http://dx.doi.org/10.4049/jimmunol.196.supp.117.10.
Testo completoAbstract (sommario):
Abstract Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil-associated diseases. Eosinophils have been proposed to play a pathologic role in the heart. Nevertheless, the pathways that recruit eosinophils to the heart have not been described. In IFNγ−/− IL-17A−/− mice, induction of experimental autoimmune myocarditis results in a Th-2-driven, eosinophilic inflammation. IFNγ−/− IL-17A−/− mice had much higher expression of the eosinophil-attracting chemokines eotaxin-1 (Ccl11) and eotaxin-2 (Ccl24) in the heart than wildtype mice. Genetic ablation of the eotaxin receptor CCR3 resulted in a dramatic decrease in heart infiltrating eosinophils. Adoptive transfer experiments with CCR3+/+ or CCR3−/− eosinophils into eosinophil-deficient ΔdblGATA1 or IFNγ−/− IL-17A−/− ΔdblGATA1 recipients showed that two conditions have to be met for efficient eosinophil trafficking to the inflamed heart: high eotaxin expression in the heart and expression of CCR3 by eosinophils. We identified the source of cardiac eotaxins by RT-PCR of FACS sorted heart cells and by immunohistochemistry. Eotaxin-1 was mainly produced by cardiac fibroblasts with interstitial localization in the heart. In vitro culture of cardiac fibroblasts with IL-4 and IL-13 induced eotaxin-1 expression. In contrast, eotaxin-2 was expressed by multiple inflammatory cell types, located at inflammatory foci, and substantial expression was only found in mice lacking IFNγ and IL-17A during myocarditis. In conclusion, eosinophil trafficking to the heart is dependent on the eotaxin-CCR3 pathway in mice with eosinophilic myocarditis. Blockade of this pathway may be a useful therapeutic approach to prevent eosinophil-mediated heart damage.
6
Rothenberg, Marc E. "Eotaxin". American Journal of Respiratory Cell and Molecular Biology 21, n. 3 (settembre 1999): 291–95. http://dx.doi.org/10.1165/ajrcmb.21.3.f160.
Testo completo
7
Jo, Jung Hyun, Yong-Tae Kim, Ho Soon Choi, Ho Gak Kim, Hong Sik Lee, Young Woo Choi, Dong Uk Kim et al. "KG 4/2015: A randomized, controlled, multicenter, open-label phase III clinical trial of GV1001 with gemcitabine/capecitabine in previous untreated, eotaxin-high patients with advanced pancreatic ductal adenocarcinoma." Journal of Clinical Oncology 39, n. 15_suppl (20 maggio 2021): 4020. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.4020.
Testo completoAbstract (sommario):
4020 Background: In the TeloVac study, GV1001 with Gemcitabine/capecitabine (G/C) did not show increased overall survival (OS) than G/C in patients (pts) with advanced pancreatic ductal adenocarcinoma (PDA). But cytokine examination suggested high serum eotaxin level may predict improved survivals in pts received GV1001 with G/C. This phase III trial was designed to assess the efficacy of GV1001 with G/C for previous untreated eotaxin-high Korean pts with advanced PDA. Methods: Eligible pts with histologically proven locally advanced and metastatic PDA (except peritoneal carcinomatosis), age > 18 years, and ECOG PS 0–2 were recruited. Pts were randomly assigned (1:1) to receive either G/C or G/C with GV1001 (G/C/GV). All pts receiving G/C/GV were with high serum eotaxin level (≥81.02 ng/mL), and the pts receiving G/C were randomly assigned again (1:1) to eotaxin-high and eotaxin-low pts. Study was designed according to Korean MFDS guidance for approval of clinical trial. G/C treatment included G (1000 mg/m2, 30 min IVF, D 1, 8, & 15) and C (830 mg/m2 BID for 21 days per month (m). G/C/GV treatment included an intradermal injection of GM-CSF (75 μg) and GV1001 (0.56 mg; D 1, 3, & 5, once on week 2–4, & 6, then monthly thereafter) from the start of G/C. The primary endpoint was OS. The secondary endpoints included time to progression (TTP), objective response rate, and safety. Survival data was analyzed using the copula graphic estimate method under dependent censoring. The response was independently assessed per RECIST v1.1. Under the one-sided significance level of 2.5% and to achieve the power of 80% of the statistical significance with the median OS difference from 7.9 to 14.9 m (HR = 0.53), 85 events and 118 registrations needed. Considering 20% drop-outs, 148 registrations were required. Results: Between Nov 2015 and Apr 2020, of 511 pts screened in 16 centers, eotaxin-high pts were identified as 34.7% (174 / 502 pts). 148 pts randomly assigned to G/C/GV (n = 75; all eotaxine-high) and G/C (n = 73; 37 eotaxine-high, 36 eotaxine-low). Median OS was significantly improved in the G/C/GV group with 11.3m [95% CI 8.6-14.0] than G/C group with 7.5 m [95% CI 5.1-10.0] (p = 0.021). Also, median TTP was significantly improved in the G/C/GV group (7.3 m [95% CI 5.0-9.7]) than in the G/C group (4.5 m [95% CI 3.2-5.8], p = 0.021). In other secondary endpoints, no statistical significance was confirmed between the two groups. Grade 3-4 treatment-emergent adverse events were reported in 49 pts (73.13%) vs. 58 pts (77.33%) in the G/C and G/C/GV group, without significant differences (p = 0.562). Conclusions: G/C/GV treatments significantly extend OS and TTP in advanced PDA than G/C, and specific safety-related issues had not been found. GV1001 should be considered as one of the options in PDA pts with high serum eotaxin levels. Clinical trial information: NCT02854072.
8
Beal, Dominic R., David M. Stepien, Sudha Natarajan, Jiyoun Kim e Daniel G. Remick. "Reduction of eotaxin production and eosinophil recruitment by pulmonary autologous macrophage transfer in a cockroach allergen-induced asthma model". American Journal of Physiology-Lung Cellular and Molecular Physiology 305, n. 11 (1 dicembre 2013): L866—L877. http://dx.doi.org/10.1152/ajplung.00120.2013.
Testo completoAbstract (sommario):
We sought to investigate the effects of cockroach allergen (CRA) exposure on the lung macrophage population to determine how different macrophage phenotypes influence exacerbation of disease. CRA exposure caused significantly reduced expression of CD86 on lung macrophages. These effects were not systemic, as peritoneal macrophage CD86 expression was not altered. To investigate whether naïve macrophages could reduce asthma-like pulmonary inflammation, autologous peritoneal macrophages were instilled into the airways 24 h before the final CRA challenge. Pulmonary inflammation was assessed by measurement of airway hyperresponsiveness, mucin production, inflammatory cell recruitment, and cytokine production. Cell transfer did not have significant effects in control mice, nor did it affect pulmonary mucin production or airway hyperresponsiveness in control or CRA-exposed mice. However, there was significant reduction in the number of eosinophils recovered in the bronchoalveolar lavage (BAL) (5.8 × 105vs. 0.88 × 105), and total cell recruitment to the airways of CRA-exposed mice was markedly reduced (1.1 × 106vs. 0.57 × 106). The reduced eosinophil recruitment was reflected by substantially lower levels of eosinophil peroxidase in the lung and significantly lower concentrations of eotaxins in BAL (eotaxin 1: 3 pg/ml vs. undetectable; eotaxin 2: 2,383 vs. 131 pg/ml) and lung homogenate (eotaxin 1: 1,043 vs. 218 pg/ml; eotaxin 2: 10 vs. 1.5 ng/ml). We conclude that CRA decreases lung macrophage CD86 expression. Furthermore, supplementation of the lung cell population with peritoneal macrophages inhibits eosinophil recruitment, achieved through reduction of eotaxin production. These data demonstrate that transfer of naïve macrophages will reduce some aspects of asthma-like pulmonary inflammation in response to CRA.
9
Forssmann, Ulf, Mariagrazia Uguccioni, Pius Loetscher, Clemens A. Dahinden, Hanno Langen, Marcus Thelen e Marco Baggiolini. "Eotaxin-2, a Novel CC Chemokine that Is Selective for the Chemokine Receptor CCR3, and Acts Like Eotaxin on Human Eosinophil and Basophil Leukocytes". Journal of Experimental Medicine 185, n. 12 (16 giugno 1997): 2171–76. http://dx.doi.org/10.1084/jem.185.12.2171.
Testo completoAbstract (sommario):
A novel human CC chemokine consisting of 78 amino acids and having a molecular mass of 8,778.3 daltons (VVIPSPCCMF FVSKRIPENR VVSYQLSSRS TCLKAGVIFT TKKGQQ SCGD PKQEWVQRYM KNLDAKQKKA SPRARAVA) was isolated together with three minor COOH-terminally truncated variants with 73, 75, and 76 residues. The new chemokine was termed eotaxin-2 because it is functionally very similar to eotaxin. In terms of structure, however, eotaxin and eotaxin-2 are rather distant, they share only 39% identical amino acids and differ almost completely in the NH2-terminal region. Eotaxin-2 induced chemotaxis of eosinophils as well as basophils, with a typically bimodal concentration dependence, and the release of histamine and leukotriene C4 from basophils that had been primed with IL-3. In all assays, eotaxin-2 had the same efficacy as eotaxin, but was somewhat less potent. The migration and the release responses were abrogated in the presence of a monoclonal antibody that selectively blocks the eotaxin receptor, CCR3, indicating that eotaxin-2, like eotaxin, acts exclusively via CCR3. Receptor usage was also studied in desensitization experiments by measuring [Ca2+]i changes in eosinophils. Complete cross-desensitization was observed between eotaxin-2, eotaxin and MCP-4 confirming activation via CCR3. No Ca2+ mobilization was obtained in neutrophils, monocytes and lymphocytes, in agreement with the lack of chemotactic responsiveness. Intradermal injection of eotaxin-2 in a rhesus monkey (100 or 1,000 pmol per site) induced a marked local infiltration of eosinophils, which was most pronounced in the vicinity of postcapillary venules and was comparable to the effect of eotaxin.
10
Struyf, Sofie, Paul Proost, Dominique Schols, Erik De Clercq, Ghislain Opdenakker, Jean-Pierre Lenaerts, Michel Detheux et al. "CD26/Dipeptidyl-Peptidase IV Down-Regulates the Eosinophil Chemotactic Potency, But Not the Anti-HIV Activity of Human Eotaxin by Affecting Its Interaction with CC Chemokine Receptor 3". Journal of Immunology 162, n. 8 (15 aprile 1999): 4903–9. http://dx.doi.org/10.4049/jimmunol.162.8.4903.
Testo completoAbstract (sommario):
Abstract Chemokines attract and activate distinct sets of leukocytes. The CC chemokine eotaxin has been characterized as an important mediator in allergic reactions because it selectively attracts eosinophils, Th2 lymphocytes, and basophils. Human eotaxin has a penultimate proline, indicating that it might be a substrate for dipeptidyl-peptidase IV (CD26/DPP IV). In this study we demonstrate that eotaxin is efficiently cleaved by CD26/DPP IV and that the NH2-terminal truncation affects its biological activity. CD26/DPP IV-truncated eotaxin(3–74) showed reduced chemotactic activity for eosinophils and impaired binding and signaling properties through the CC chemokine receptor 3. Moreover, eotaxin(3–74) desensitized calcium signaling and inhibited chemotaxis toward intact eotaxin. In addition, HIV-2 infection of CC chemokine receptor 3-transfected cells was inhibited to a similar extent by eotaxin and eotaxin(3–74). Thus, CD26/DPP IV differently regulates the chemotactic and antiviral potencies of eotaxin by the removal of two NH2-terminal residues. This physiological processing may be an important down-regulatory mechanism, limiting eotaxin-mediated inflammatory responses.
11
Komiya, A., H. Nagase, H. Yamada, T. Sekiya, M. Yamaguchi, Y. Sano, N. Hanai et al. "Concerted expression of eotaxin-1, eotaxin-2, and eotaxin-3 in human bronchial epithelial cells". Journal of Allergy and Clinical Immunology 111, n. 2 (febbraio 2003): S150. http://dx.doi.org/10.1016/s0091-6749(03)80481-5.
Testo completo
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Komiya, Akiko, Hiroyuki Nagase, Hirokazu Yamada, Takashi Sekiya, Masao Yamaguchi, Yasuyuki Sano, Nobuo Hanai et al. "Concerted expression of eotaxin-1, eotaxin-2, and eotaxin-3 in human bronchial epithelial cells". Cellular Immunology 225, n. 2 (ottobre 2003): 91–100. http://dx.doi.org/10.1016/j.cellimm.2003.10.001.
Testo completo
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Ruth, Jeffrey H., Nicholas W. Lukacs, Kelly S. Warmington, Tim J. Polak, Marie Burdick, Steven L. Kunkel, Robert M. Strieter e Stephen W. Chensue. "Expression and Participation of Eotaxin During Mycobacterial (Type 1) and Schistosomal (Type 2) Antigen-Elicited Granuloma Formation". Journal of Immunology 161, n. 8 (15 ottobre 1998): 4276–82. http://dx.doi.org/10.4049/jimmunol.161.8.4276.
Testo completoAbstract (sommario):
Abstract Eotaxin participation was analyzed during types 1 and 2 lung granuloma formation induced by embolizing Sepharose beads coupled to purified protein derivative (PPD) of Mycobacterium bovis or soluble Ags derived from Schistosoma mansoni eggs. Eotaxin was monitored by protein ELISA and semiquantitative reverse-transcriptase PCR mRNA analysis. Both types 1 and 2 granulomas released eotaxin, but levels were sixfold greater (on day 4) in the type 2 than for the type 1 or foreign body granulomas. Transcripts for eotaxin, IL-4, and CCR3 (eotaxin receptor) were also enhanced during type 2 granuloma formation. Anti-IL-4 treatment impaired eotaxin mRNA in lungs with type 2 granulomas, indicating that IL-4 promoted local eotaxin expression. In vivo, anti-eotaxin treatment caused modest reductions in the size of both types 1 and 2 lesions, with negligible effect on eosinophil recruitment. Surprisingly, anti-eotaxin treatment abrogated IFN-γ-producing cells in regional lymph nodes during the type 1 PPD response. Lymph nodes draining both types 1 and 2 lesions showed enhanced CCR3 mRNA, but this followed the time of maximum eotaxin protein and mRNA expression. Correlative, in vitro studies revealed that graded doses of eotaxin increased IFN-γ production from PPD-sensitive regional lymph node cultures, while monocyte-chemotactic protein-1, an important macrophage chemoattractant, had the opposite effect. These findings indicate that eotaxin expression is not limited to type 2 hypersensitivity granulomas, but also promotes IFN-γ production during mycobacterial responses.
14
Khoury, Tawfik, Dory Rotnemer-Golinkin, Lidya Zolotarev e Yaron Ilan. "Orally administered anti-eotaxin-1 monoclonal antibody is biologically active in the gut and alleviates immune-mediated hepatitis: A novel anti-inflammatory personalized therapeutic approach". International Journal of Immunopathology and Pharmacology 35 (gennaio 2021): 205873842110212. http://dx.doi.org/10.1177/20587384211021215.
Testo completoAbstract (sommario):
Personalized therapies are designed to optimize the safety-to-efficacy ratio by selecting patients with higher response rates based on specific biomarkers. Inflammation plays a vital role in the pathogenesis of non-alcoholic steatohepatitis (NASH), a common liver disorder. Eotaxin-1 plays a role in innate and adaptive immune responses. High eotaxin-1 levels are associated with diabetes and fatty liver disease and, therefore, serves as a biomarker for patient selection. The anti-eotaxin-1 monoclonal antibody is tailored for the personalized therapy of patients with inflammatory conditions due to high levels of eotaxin-1. To evaluate the biological activity and immunomodulatory effect of orally administered anti-eotaxin-1. C57B1/6 mice were treated with either oral or intra-peritoneal anti-eotaxin-1 antibody before induction of immune-mediated hepatitis using an injection of concanavalin A (ConA) and checked for liver injury and eotaxin-1 serum levels. Oral administration of anti-eotaxin-1 alleviated the immune-mediated liver injury. Serum alanine aminotransferase levels decreased to 1807 U/L, compared with 19025 U/L in untreated controls and 3657 U/L in mice treated with parenteral anti-eotaxin-1 ( P < 0.005). A trend toward reduced serum eotaxin-1 levels was observed in treated mice, ranging from 594 pg/mL in the controls to 554 and 561 pg/mL in mice treated orally and intraperitoneally ( P = 0.08, P = 0.06, respectively). Oral administration of anti-eotaxin-1 antibody shows biological activity in the gut and exerts a systemic immunomodulatory effect to alleviate immune-mediated hepatitis. The data suggest that testing for eotaxin-1 serum levels may enable screening patients with high-eotaxin-1 levels-associated NASH.
15
Tenscher, K., B. Metzner, E. Schopf, J. Norgauer e W. Czech. "Recombinant human eotaxin induces oxygen radical production, Ca(2+)- mobilization, actin reorganization, and CD11b upregulation in human eosinophils via a pertussis toxin-sensitive heterotrimeric guanine nucleotide-binding protein". Blood 88, n. 8 (15 ottobre 1996): 3195–99. http://dx.doi.org/10.1182/blood.v88.8.3195.bloodjournal8883195.
Testo completoAbstract (sommario):
The novel human CC-chemokine Eotaxin is a potent and selective chemotaxin for eosinophils. Here, the biological activities and the activation profile of Eotaxin were further characterized and compared with those of other eosinophil chemotaxins such as complement fragment C5a (C5a), platelet-activating factor (PAF), and RANTES in human eosinophils. Eotaxin stimulated the production of reactive oxygen metabolites as shown by lucigenin-dependent chemiluminescence and superoxide dismutase-inhibitable cytochrome C reduction. Furthermore, Eotaxin induced upregulation of the integrin CD11b. In addition, fluorescence measurements with Fura-2-labeled eosinophils in the presence of EGTA indicated Ca(2+)-mobilization from intracellular stores by Eotaxin. Flow cytometric studies showed rapid and translent actin polymerization on stimulation with Eotaxin. At optimal concentrations, the changes induced by Eotaxin were comparable with those obtained by C5a, PAF, and RANTES. Call responses elicited by Eotaxin were inhibited by pertussis toxin, indicating coupling of its putative receptor to heterotrimeric guanine nucleotide-binding proteins. These results indicate that Eotaxin is a strong activator of eosinophils with biological activity comparable with those of the eosinophil chemotaxins C5a, PAF, and RANTES. These findings point to a role of Eotaxin in the pathogenesis of eosinophilic inflammation as a chemotaxin as well as an activator of proinflammatory effector functions.
16
Das, A. M., R. J. Flower e M. Perretti. "Eotaxin-induced eosinophil migration in the peritoneal cavity of ovalbumin-sensitized mice: mechanism of action." Journal of Immunology 159, n. 3 (1 agosto 1997): 1466–73. http://dx.doi.org/10.4049/jimmunol.159.3.1466.
Testo completoAbstract (sommario):
Abstract Cell accumulation in response to i.p. administration of the C-C chemokine, eotaxin, was studied in vivo. OVA-sensitized mice, exhibiting blood eosinophilia, had greater eosinophil (Eø) accumulation in response to 500 ng of eotaxin at 6 h (vehicle-injected, 3.0 +/- 0.5 x 10(5); eotaxin-injected, 8.6 +/- 1.0 x 10(5)) than nonsensitized, eotaxin-injected mice (2.5 +/- 0.4 x 10(5)). A nonspecific neutrophil migration was observed in both vehicle- and eotaxin-injected cavities. The number of intact mast cells in the peritoneal lavages after eotaxin injection was significantly lower than that in vehicle-injected animals (0.8 +/- 0.3 x 10(4) vs 2.8 +/-0.6 x 10(4), respectively). When endogenous peritoneal mast cells were depleted with compound 48/80 before eotaxin administration, there was a 51% reduction in Eø accumulation. This suggests an important role for endogenous mast cells in mediating the actions of eotaxin. The potential role of mast cell mediators in the actions of eotaxin was also investigated. Pretreatment with histamine-H1 or serotonin antagonists reduced Eø migration in response to eotaxin by 50 to 65%. Further, following pretreatment with a specific mAb against TNF-alpha, only nonspecific neutrophil influx was attenuated. Using neutralizing mAbs, Eø migration was found to be dependent on the adhesion molecules P- and E-selectin and CD11b. Eø accumulation was also sensitive to dexamethasone, with doses as low as 0.2 mg/kg inducing 100% inhibition. This study provides useful insight into the mechanisms of action of eotaxin.
17
Marleau, S., D. A. Griffiths-Johnson, P. D. Collins, Y. S. Bakhle, T. J. Williams e P. J. Jose. "Human RANTES acts as a receptor antagonist for guinea pig eotaxin in vitro and in vivo." Journal of Immunology 157, n. 9 (1 novembre 1996): 4141–46. http://dx.doi.org/10.4049/jimmunol.157.9.4141.
Testo completoAbstract (sommario):
Abstract The guinea pig C-C chemokine, eotaxin, is a potent and selective eosinophil chemoattractant in guinea pig airways and skin in vivo, and stimulates both guinea pig and human eosinophils in vitro. The human C-C chemokine RANTES (30% homology with guinea pig eotaxin) stimulates human eosinophils in vitro, but does not stimulate guinea pig eosinophils, even though these cells bind 125I-RANTES. Similar concentrations of eotaxin and unlabeled RANTES competitively inhibit the binding of 125I-RANTES to guinea pig eosinophils, suggesting that eotaxin and RANTES share a common binding site on these cells. In the present study, we investigated the possibility that human RANTES, binding to a putative eotaxin receptor on guinea pig eosinophils, might block functional responses to eotaxin. When fura-2-loaded cells were first exposed to RANTES, which failed to elevate the intracellular calcium concentration, the response to a subsequent challenge with eotaxin was inhibited in a dose-dependent manner. Inhibition was also demonstrated when the two chemokines were added simultaneously. Another human C-C chemokine, MCP-3 (52% homology with guinea pig eotaxin), had similar inhibitory effects on the eotaxin-induced activation of guinea pig eosinophils in vitro. RANTES inhibited (111)In-eosinophil accumulation in response to intradermal eotaxin in vivo. In contrast, RANTES had no significant effect on responses to leukotriene B4 in vitro or in vivo. Thus, these experiments in the guinea pig demonstrate that human RANTES is the first prototypic antagonist of an eotaxin receptor.
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Olze, H., U. Förster, T. Zuberbier, L. Morawietz e E. O. Luger. "Eotaxin-, Eotaxin-2-, Eotaxin-3- und RANTES-Proteinsynthese bei Polyposis nasi Korrelation zu Eosinophilie und Ätiologie". Allergologie 29, n. 03 (1 marzo 2006): 77–85. http://dx.doi.org/10.5414/alp29077.
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Luz, Ricardo Alves, Pedro Xavier-Elsas, Bianca de Luca, Daniela Masid-de-Brito, Priscila Soares Cauduro, Luiz Carlos Gondar Arcanjo, Ana Carolina Cordeiro Faria dos Santos, Ivi Cristina Maria de Oliveira e Maria Ignez Capella Gaspar-Elsas. "5-Lipoxygenase-Dependent Recruitment of Neutrophils and Macrophages by Eotaxin-Stimulated Murine Eosinophils". Mediators of Inflammation 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/102160.
Testo completoAbstract (sommario):
The roles of eosinophils in antimicrobial defense remain incompletely understood. In ovalbumin-sensitized mice, eosinophils are selectively recruited to the peritoneal cavity by antigen, eotaxin, or leukotriene(LT)B4, a 5-lipoxygenase (5-LO) metabolite. 5-LO blockade prevents responses to both antigen and eotaxin. We examined responses to eotaxin in the absence of sensitization and their dependence on 5-LO. BALB/c or PAS mice and their mutants (5-LO-deficient ALOX; eosinophil-deficient GATA-1) were injected i.p. with eotaxin, eosinophils, or both, and leukocyte accumulation was quantified up to 24 h. Significant recruitment of eosinophils by eotaxin in BALB/c, up to 24 h, was accompanied by much larger numbers of recruited neutrophils and monocytes/macrophages. These effects were abolished by eotaxin neutralization and 5-LO-activating protein inhibitor MK886. In ALOX (but not PAS) mice, eotaxin recruitment was abolished for eosinophils and halved for neutrophils. In GATA-1 mutants, eotaxin recruited neither neutrophils nor macrophages. Transfer of eosinophils cultured from bone-marrow of BALB/c donors, or from ALOX donors, into GATA-1 mutant recipients, i.p., restored eotaxin recruitment of neutrophils and showed that the critical step dependent on 5-LO is the initial recruitment of eosinophils by eotaxin, not the secondary neutrophil accumulation. Eosinophil-dependent recruitment of neutrophils in naive BALB/c mice was associated with increased binding of bacteria.
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Ogilvie, Patricia, Giuseppe Bardi, Ian Clark-Lewis, Marco Baggiolini e Mariagrazia Uguccioni. "Eotaxin is a natural antagonist for CCR2 and an agonist for CCR5". Blood 97, n. 7 (1 aprile 2001): 1920–24. http://dx.doi.org/10.1182/blood.v97.7.1920.
Testo completoAbstract (sommario):
Abstract Eotaxin is a potent inducer of eosinophil chemotaxis and was considered as a selective ligand of the CC chemokine receptor 3 (CCR3), which is expressed on eosinophils, basophils, and Th2 lymphocytes. This study shows that eotaxin also interacts with CCR2 and CCR5 and can, thus, affect the responses of monocytes, which express both receptors. In human monocytes pretreatment with eotaxin decreased responsiveness to MCP-1, a selective ligand for CCR2, as well as to RANTES and MIP-1β, which bind to CCR5. Similar effects were obtained with transfected cells expressing CCR2 or CCR5, but here a difference became apparent: Eotaxin triggered CCR5 at a concentration of 100 nM but not CCR2 even at 1 μM, suggesting an antagonistic effect on this receptor. In agreement with this observation, eotaxin induced internalization of CCR5 but not of CCR2 in human monocytes and transfected cells. Binding studies showed that eotaxin displaces125 I-MCP-1 from monocytes in a concentration-dependent manner, and functional experiments showed that eotaxin inhibits MCP-1-induced chemotaxis and enzyme release. The results demonstrate that eotaxin is a CCR5 agonist and a CCR2 antagonist. The present findings suggest a role of eotaxin in the fine-tuning of cellular responses occurring at sites of allergic inflammation, in which both MCP-1 and eotaxin are produced.
21
Ying, Sun, Douglas S. Robinson, Qiu Meng, Luis T. Barata, Alan R. McEuen, Mark G. Buckley, Andrew F. Walls, Philip W. Askenase e A. Barry Kay. "C-C Chemokines in Allergen-Induced Late-Phase Cutaneous Responses in Atopic Subjects: Association of Eotaxin with Early 6-Hour Eosinophils, and of Eotaxin-2 and Monocyte Chemoattractant Protein-4 with the Later 24-Hour Tissue Eosinophilia, and Relationship to Basophils and Other C-C Chemokines (Monocyte Chemoattractant Protein-3 and RANTES)". Journal of Immunology 163, n. 7 (1 ottobre 1999): 3976–84. http://dx.doi.org/10.4049/jimmunol.163.7.3976.
Testo completoAbstract (sommario):
Abstract The relationship of expression of the C-C chemokines eotaxin, eotaxin 2, RANTES, monocyte chemoattractant protein-3 (MCP-3), and MCP-4 to the kinetics of infiltrating eosinophils, basophils, and other inflammatory cells was examined in allergen-induced, late-phase allergic reactions in the skin of human atopic subjects. EG2+ eosinophils peaked at 6 h and correlated significantly with eotaxin mRNA and protein, whereas declining eosinophils at 24 h correlated significantly with eotaxin-2 and MCP-4 mRNA. In contrast, no significant correlations were observed between BB1+ basophil infiltrates, which peaked at 24 h, and expression of eotaxin, eotaxin-2, RANTES, MCP-3, and MCP-4 or elastase+ neutrophils (6-h peak), CD3+ and CD4+ T cells (24 h), and CD68+ macrophages (72 h). Furthermore, 83% of eosinophils, 40% of basophils, and 1% of CD3+ cells expressed the eotaxin receptor CCR3, while eotaxin protein was expressed by 43% of macrophages, 81% of endothelial cells, and 6% of T cells (6%). These data suggest that 1) eotaxin has a role in the early 6-h recruitment of eosinophils, while eotaxin-2 and MCP-4 appear to be involved in later 24-h infiltration of these CCR3+ cells; 2) different mechanisms may guide the early vs late eosinophilia; and 3) other chemokines and receptors may be involved in basophil accumulation of allergic tissue reactions in human skin.
22
Ogilvie, Patricia, Samantha Paoletti, Ian Clark-Lewis e Mariagrazia Uguccioni. "Eotaxin-3 is a natural antagonist for CCR2 and exerts a repulsive effect on human monocytes". Blood 102, n. 3 (1 agosto 2003): 789–94. http://dx.doi.org/10.1182/blood-2002-09-2773.
Testo completoAbstract (sommario):
Abstract Eotaxin-3 (CCL26) belongs to the group of CC chemokines that attract eosinophils, basophils, and Th2 lymphocytes. Like eotaxin (CCL11) and eotaxin-2 (CCL24), eotaxin-3 mediates its activity through CCR3. Here we show that eotaxin-3 also binds to CCR2 on monocytes and CCR2-transfected cells. In contrast to monocyte chemotactic protein 1 (MCP-1; CCL2), eotaxin-3 does not trigger intracellular calcium mobilization, enzyme release, or phosphorylation of the mitogen-activated protein (MAP) kinase ERK and induces a weak chemotaxis in monocytes. Instead, eotaxin-3 inhibits MCP-1–mediated responses, thus acting as a natural antagonist for CCR2. This study also demonstrates that eotaxin-3 promotes active movement of monocytes away from a gradient of eotaxin-3 in vitro. This repellent effect is amplified when an additional gradient of MCP-1 is applied, demonstrating that the 2 mechanisms are synergistic. Eotaxin-3 effects on monocytes are largely abolished when cells are pretreated with MCP-1 or CCR2 antagonists. Like MCP-1–mediated migration, repulsion is sensitive to Bordetella pertussis toxin, indicating the involvement of Gi protein–coupled receptors. However, using transfected cells expressing CCR2 we could not detect F-actin formation or an active movement away induced by eotaxin-3, suggesting that either expression of a single receptor type is not sufficient to mediate cell repulsion or that the used transfected cell lines lack additional interaction molecules that are required for reverse migration. Eotaxin-3 was expressed by vascular endothelial cells and was essential for endothelial transmigration of eosinophils. Our data provide a mechanism by which 2 chemokine gradients that are oriented in opposite directions could cooperate in efficiently driving out monocytes from blood vessels into tissue.
23
Ishii, Yukio, Manabu Shirato, Akihiro Nomura, Tohru Sakamoto, Yoshiyuki Uchida, Morio Ohtsuka, Masaru Sagai e Shizuo Hasegawa. "Cloning of rat eotaxin: ozone inhalation increases mRNA and protein expression in lungs of Brown Norway rats". American Journal of Physiology-Lung Cellular and Molecular Physiology 274, n. 1 (1 gennaio 1998): L171—L176. http://dx.doi.org/10.1152/ajplung.1998.274.1.l171.
Testo completoAbstract (sommario):
The C-C chemokine eotaxin is thought to be important in the selective recruitment of eosinophils to the site of inflammation in guinea pigs, mice, and humans. We isolated the rat eotaxin gene to determine whether a similar molecule might play a role in the pulmonary infiltration of eosinophils during acute inflammation in the rat. The cDNA for rat eotaxin encoded a 97-amino acid protein containing a 74-amino acid mature eotaxin protein with 97.3% identity to mouse eotaxin. The recombinant protein encoded by this gene displayed specific chemotactic activity for eosinophils when analyzed with a microchemotactic chamber. The expression of eotaxin mRNA increased ∼1.6-fold immediately after exposure to ozone and was 4-fold higher after 20 h. The number of lavageable eosinophils at the same time points were 3- and 15-fold greater, respectively, than control eosinophils. Immunocytochemistry revealed that alveolar macrophages and bronchial epithelial cells were positive for eotaxin. These results suggest that eotaxin may be involved in the recruitment of eosinophils into the air spaces during certain inflammatory conditions in rats.
24
Koç, Ümit, Erdinç Çetinkaya, Erdal B. Bostanci, Ahu S. Kemık, Mesut Tez, İsmail Gömceli e Musa Akoğlu. "Diagnostic Significance of Serum Eotaxin-1 Level in Gastric Cancer Patients". Disease Markers 35 (2013): 363–67. http://dx.doi.org/10.1155/2013/274515.
Testo completoAbstract (sommario):
Introduction. Gastric cancer is the second cause of cancer-related deaths worldwide. Delayed diagnosis leads to high mortality rates. Eotaxin-1 was originally discovered as an eosinophil-selective chemoattractant and may play a role in a number of chronic inflammatory diseases, cancer, and other gastrointestinal disorders. The aim of this study was to analyse diagnostic and prognostic significance of serum eotaxin-1 (s-eotaxin-1) levels in gastric cancer.Methods. Sixty gastric cancer patients and 69 healthy subjects were included into the study. S-eotaxin-1 levels were compared with clinicopathological features and outcomes in gastric cancer.Results. Serum levels of eotaxin-1 in gastric cancer patients were significantly higher than controls ( pg/mL versus pg/mL, respectively ()). The s-eotaxin-1 levels did not differ significantly with histopathological grade, tumor-node-metastasis (TNM) stage, tumor localization, lymph node metastases, positive lymph node ratio, size, perineural and perivascular invasion. So there is no relationship found between s-eotaxin-1 level and prognosis.Conclusion. S-eotaxin-1 levels may be used as an easily available biomarker for gastric cancer risk and may alert physicians for early diagnosis. Due to the limited number of patients included in this study, larger cohort studies are warranted to validate the diagnostic value of s-eotaxin-1 level in gastric cancer.
25
Franz-Bacon, Karin, Daniel J. Dairaghi, Stefen A. Boehme, Susan K. Sullivan, Thomas J. Schall, Paul J. Conlon, Naomi Taylor e Kevin B. Bacon. "Human Thymocytes Express CCR-3 and Are Activated by Eotaxin". Blood 93, n. 10 (15 maggio 1999): 3233–40. http://dx.doi.org/10.1182/blood.v93.10.3233.410k33_3233_3240.
Testo completoAbstract (sommario):
Eotaxin has been characterized as a chemokine involved in eosinophil activation; however, mRNA for this C-C chemokine has been shown to be constitutively expressed in thymus. Immunohistochemical analysis showed a punctate distribution pattern, with eotaxin expression localized mainly in the medulla and in Hassle’s corpuscles. Moreover, the receptor for eotaxin, CCR-3, was detected on thymocytes, with the highest level of expression being on the CD8 single-positive population. Equilibrium binding analyses on unfractionated thymocytes demonstrated specific 125I-eotaxin binding profiles comparable with CCR-3 transfectants. Eotaxin induced cell migration and mobilization of intracellular calcium in all thymocytes except the immature CD4−/CD8− population. Eotaxin also induced the secretion of the chemokines interleukin-8, RANTES, and macrophage inflammatory protein-1β from thymocyte cultures in vitro. These results suggest that eotaxin-induced thymocyte activation may have important physiological implications for lymphocyte mobilization within and from this lymphoid organ.
26
Rothenberg, M. E., A. D. Luster, C. M. Lilly, J. M. Drazen e P. Leder. "Constitutive and allergen-induced expression of eotaxin mRNA in the guinea pig lung." Journal of Experimental Medicine 181, n. 3 (1 marzo 1995): 1211–16. http://dx.doi.org/10.1084/jem.181.3.1211.
Testo completoAbstract (sommario):
Eotaxin is a member of the C-C family of chemokines and is related during antigen challenge in a guinea pig model of allergic airway inflammation (asthma). Consistent with its putative role in eosinophilic inflammation, eotaxin induces the selective infiltration of eosinophils when injected into the lung and skin. Using a guinea pig lung cDNA library, we have cloned full-length eotaxin cDNA. The cDNA encodes a protein of 96 amino acids, including a putative 23-amino acid hydrophobic leader sequence, followed by 73 amino acids composing the mature active eotaxin protein. The protein-coding region of this cDNA is 73, 71, 50, and 48% identical in nucleic acid sequence to those of human macrophage chemoattractant protein (MCP) 3, MCP-1, macrophage inflammatory protein (MIP) 1 alpha, and RANTES, respectively. Analysis of genomic DNA suggested that there is a single eotaxin gene in guinea pig which is apparently conserved in mice. High constitutive levels of eotaxin mRNA expression were observed in the lung, while the intestines, stomach, spleen, liver, heart, thymus, testes, and kidney expressed lower levels. To determine if eotaxin mRNA levels are elevated during allergen-induced eosinophilic airway inflammation, ovalbumin (OVA)-sensitized guinea pigs were challenged with aerosolized antigen. Compared with the lungs from saline-challenged animals, eotaxin mRNA levels increased sixfold within 3 h and returned to baseline by 6 h. Thus, eotaxin mRNA levels are increased in response to allergen challenge during the late phase response. The identification of constitutive eotaxin mRNA expression in multiple tissues suggests that in addition to regulating airway eosinophilia, eotaxin is likely to be involved in eosinophil recruitment into other tissues as well as in baseline tissue homing.
27
Yang, Yi, James Loy, Rolf-Peter Ryseck, Daniel Carrasco e Rodrigo Bravo. "Antigen-Induced Eosinophilic Lung Inflammation Develops in Mice Deficient in Chemokine Eotaxin". Blood 92, n. 10 (15 novembre 1998): 3912–23. http://dx.doi.org/10.1182/blood.v92.10.3912.422k23_3912_3923.
Testo completoAbstract (sommario):
The mechanisms that regulate the selective infiltration of eosinophils in certain allergic diseases are still poorly understood. The CC chemokine eotaxin is a potent chemoattractant, highly specific for eosinophils. Recent studies have implicated that eotaxin plays an important role in the recruitment of eosinophils in different inflammation processes. A number of other chemokines, cytokines, and chemoattractants also have chemotactic activities for eosinophils and some of them present high selectivity for eosinophils. To further study the role of eotaxin in inflammation, we generated mutant mice with the eotaxin gene disrupted and replaced by the Escherichia coliβ-galactosidase gene. These mice developed normally and had no histologic or hematopoietic abnormalities. Furthermore, our studies showed that the lack of eotaxin did not affect the recruitment of eosinophils in the inflammation models induced by Sephadex beads and thioglycollate, as well as in an experimental lung eosinophilia model induced by ovalbumin aerosol challenge, even at the onset of the inflammatory response. The replacement of the eotaxin gene by the β-galactosidase gene provided a useful marker to monitor the activity of the eotaxin promoter under normal conditions and after antigen challenges. Immunohistochemical staining suggested that endothelial cells were the major sources of eotaxin expression.
28
Rothenberg, Marc E., James A. MacLean, Eric Pearlman, Andrew D. Luster e Philip Leder. "Targeted Disruption of the Chemokine Eotaxin Partially Reduces Antigen-induced Tissue Eosinophilia". Journal of Experimental Medicine 185, n. 4 (17 febbraio 1997): 785–90. http://dx.doi.org/10.1084/jem.185.4.785.
Testo completoAbstract (sommario):
The chemokines are a large group of chemotactic cytokines that regulate leukocyte trafficking and have recently been shown to inhibit human immunodeficiency virus entry into cells. Eotaxin is a C–C chemokine implicated in the recruitment of eosinophils in a variety of inflammatory disorders and, unlike all other eosinophil chemoattractants, is eosinophil specific. However, given the large number of chemoattractants that have activities on eosinophils, it is unclear whether eotaxin has an important role in vivo. Furthermore, it remains unclear why there is constitutive expression of eotaxin in healthy states in the absence of eosinophilic inflammation. To begin to determine the significance of eotaxin at baseline and during eosinophil-mediated disease processes, we have used targeted gene disruption to generate mice that are deficient in eotaxin. Such mice demonstrate that eotaxin enhances the magnitude of the early (but not late) eosinophil recruitment after antigen challenge in models of asthma and stromal keratitis. Surprisingly, a role for eotaxin in regulating the constitutive number of eosinophils in the peripheral circulation is also demonstrated. These results indicate a contributory role for eotaxin in the generation of peripheral blood and antigen-induced tissue eosinophilia.
29
Vasudevan, Abu R., Huaizhu Wu, Antonios M. Xydakis, Peter H. Jones, E. O’Brian Smith, John F. Sweeney, David B. Corry e Christie M. Ballantyne. "Eotaxin and Obesity". Journal of Clinical Endocrinology & Metabolism 91, n. 1 (gennaio 2006): 256–61. http://dx.doi.org/10.1210/jc.2005-1280.
Testo completo
30
Pease, J. "Eotaxin and asthma". Current Opinion in Pharmacology 1, n. 3 (1 giugno 2001): 248–53. http://dx.doi.org/10.1016/s1471-4892(01)00044-3.
Testo completo
31
Devouassoux, Gilles, Dean D. Metcalfe e Calman Prussin. "Eotaxin Potentiates Antigen-Dependent Basophil IL-4 Production". Journal of Immunology 163, n. 5 (1 settembre 1999): 2877–82. http://dx.doi.org/10.4049/jimmunol.163.5.2877.
Testo completoAbstract (sommario):
Abstract Basophils are a major source of IL-4, which is a critical factor in the generation of allergic inflammation. Eotaxin induces chemotaxis mediated through the CC chemokine receptor 3 (CCR3) present on basophils as well as eosinophils and Th2 cells, thereby promoting cell recruitment. To determine whether eotaxin has other proinflammatory activity, we examined the effect of eotaxin on basophil IL-4 expression by flow cytometry. Eotaxin alone had no effect on basophil IL-4 production, but further increased allergen-stimulated IL-4 expression. Eotaxin also enhanced IL-4 release from purified basophils 2- to 4-fold, as determined by ELISA (p < 0.01). Addition of eotaxin to cultures resulted in a 40-fold left shift in the dose response to Ag. This effect was obtained with physiologic concentrations of eotaxin (10 ng/ml), was abrogated by an Ab to the CCR3 receptor, and was noted with other chemokine ligands of CCR3. Additionally, eotaxin augmented IL-3 priming of basophil IL-4 production in a synergistic manner (p < 0.01). In contrast, no priming was observed with either IL-5 or GM-CSF. These results establish a novel function for eotaxin and other chemokine ligands of CCR3: the potentiation of Ag-mediated IL-4 production in basophils, and suggest a potential nonchemotactic role for CC chemokines in the pathogenesis and amplification of inflammation.
32
Matsukura, Satoshi, Cristiana Stellato, James R. Plitt, Carol Bickel, Katsushi Miura, Steve N. Georas, Vincenzo Casolaro e Robert P. Schleimer. "Activation of Eotaxin Gene Transcription by NF-κB and STAT6 in Human Airway Epithelial Cells". Journal of Immunology 163, n. 12 (15 dicembre 1999): 6876–83. http://dx.doi.org/10.4049/jimmunol.163.12.6876.
Testo completoAbstract (sommario):
Abstract The C-C chemokine eotaxin is a potent chemoattractant for eosinophils and probably plays an important role in the pathogenesis of asthma, although the mechanisms of its regulation are not well known. Airway epithelial cells express eotaxin mRNA and protein after stimulation with a variety of cytokines. We focused on the molecular mechanisms of eotaxin gene regulation by TNF-α and IL-4 in the airway epithelial cell line, BEAS-2B. Cells were transfected with luciferase reporter plasmids, which contained up to 1363 bp of the eotaxin promoter. Eotaxin promoter activity was increased by TNF-α (2.5-fold) and IL-4 (1.5-fold), respectively. The combination of TNF-α and IL-4 produced 3.6-fold activation of the eotaxin promoter. The eotaxin promoter contains overlapping consensus binding sites for transcription factors, NF-κB and STAT6, which are known to mediate responses to TNF-α and IL-4, respectively. Electrophoretic mobility shift assays revealed NF-κB binding after TNF-α stimulation and STAT6 binding after IL-4 stimulation using a DNA probe derived from the eotaxin promoter. Mutant plasmids were generated to define the roles of these transcription factors in eotaxin promoter activity. TNF-α stimulation, but not IL-4 stimulation, was lost in plasmids mutated at the NF-κB binding site, whereas IL-4 stimulation, but not TNF-α stimulation, was lost in plasmids mutated at the STAT6 binding site. When both sites were mutated, all transcriptional activation was lost. These results imply that TNF-α and IL-4 stimulate expression of the eotaxin gene by activating NF-κB and STAT6.
33
Li, Bei, Yi-Li Zhang e Shou-Yi Yu. "Synovial Fluid Eotaxin-1 Levels May Reflect Disease Progression in Primary Knee Osteoarthritis Among Elderly Han Chinese: A Cross-Sectional Study". CARTILAGE 10, n. 4 (22 marzo 2018): 408–16. http://dx.doi.org/10.1177/1947603518764280.
Testo completoAbstract (sommario):
Objective The CC chemokine family member eotaxin-1, also named chemokine C-C motif ligand 11 (CCL11), has been detected in knee osteoarthritis (OA) and could induce breakdown of cartilage matrix. This study was performed to investigate the plasma and synovial fluid eotaxin-1 levels with the disease progression in elderly Han Chinese with primary knee OA. Design A total of 143 elderly primary knee OA patients and 135 healthy controls were enrolled in the study. The Western Ontario and McMaster Universities Arthritis Index (WOMAC) was performed to evaluate the clinical severity. The radiographic severity was assessed by Kellgren-Lawrence (K-L) grading. Plasma and synovial fluid (SF) eotaxin-1 levels were explored using enzyme-linked immunosorbent assay. The SF levels of matrix metalloproteinase–3 (MMP-3) and interleukin-6 (IL-6) were also examined. Results Elevated plasma eotaxin-1 levels were found in knee OA patients compared with healthy controls. Eotaxin-1 levels in SF of knee OA patients with K-L grade 4 were significantly elevated compared with those with K-L grades 2 and 3. Meanwhile, knee OA patients with K-L grade 3 had significantly increased SF levels of eotaxin-1 compared with those with K-L grade 2. Plasma eotaxin-1 levels in different K-L grading did not reach significant difference. Eotaxin-1 levels in SF of knee OA patients were significantly associated with disease severity evaluated by KL grading criteria. In addition, eotaxin-1 levels in SF were positively related to clinical severity illustrated by WOMAC as well as biochemical markers MMP-3 and IL-6. Conclusions Eotaxin-1 levels in SF instead of plasma, were independently and positively related to the disease severity in elderly knee OA patients. The inhibition of eotaxin-1 and its related signaling pathways may serve as a novel therapeutic approach for OA progression.
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Sanz, Maria-Jesus, Paul D. Ponath, Charles R. Mackay, Walter Newman, Masayuki Miyasaka, Tayuka Tamatani, Brian F. Flanagan et al. "Human Eotaxin Induces α4 and β2 Integrin-Dependent Eosinophil Accumulation in Rat Skin In Vivo: Delayed Generation of Eotaxin in Response to IL-4". Journal of Immunology 160, n. 7 (1 aprile 1998): 3569–76. http://dx.doi.org/10.4049/jimmunol.160.7.3569.
Testo completoAbstract (sommario):
Abstract The CC chemokine eotaxin, originally purified from bronchoalveolar lavage fluid of sensitized guinea pigs following allergen challenge, is a potent eosinophil-selective chemoattractant. In the present study, we have used 111In-eosinophils and human eotaxin to characterize the profile of chemokine-induced eosinophil accumulation in vivo in rat skin. Intradermally injected eotaxin caused a dose-dependent accumulation of 111In-eosinophils. Time course studies indicated that the response was rapid, since all the accumulation occurred within the first 1 to 2 h of eotaxin injection. The i.v. administration of anti-intercellular adhesion molecule-1, anti-vascular cell adhesion molecule-1, or anti-α4 integrin mAbs significantly inhibited the eosinophil accumulation induced by 100 pmol of human eotaxin by 73, 43, and 67%, respectively. Further, when 111In-eosinophils were pretreated in vitro with anti-α4 integrin or anti-β2 integrin mAbs, or with a combination of both mAbs, eotaxin-induced responses in vivo were reduced by 52, 49, and 68%, respectively. Eosinophil accumulation induced by intradermal IL-4, but not that induced by TNF-α or leukotriene B4, appeared to be mediated in part by endogenously generated eotaxin. Anti-eotaxin Abs significantly inhibited (54%) the later phases (24–28 h) but not the early phase (0–4 h) of the response to IL-4. This was consistent with eotaxin mRNA expression peaking at 18 h after IL-4 injection. Our findings show that human eotaxin is a potent inducer of eosinophil accumulation in vivo, this response being dependent on α4 integrin/vascular cell adhesion molecule-1 and β2 integrin/intercellular adhesion molecule-1 adhesion pathways. Further, the eosinophil accumulation in response to IL-4 is partly mediated by endogenously generated eotaxin.
35
Meng, Qiu, Andrew Menzies-Gow, Simon Phipps, richard Stillion, A. Barry Kay e Sun Ying. "Intracutaneous eotaxin and eotaxin-2 induces mRNA expression of IL-4, IL-5, eotaxin and eotaxin-2 in human atopic and non-atopic subjects". Journal of Allergy and Clinical Immunology 109, n. 1 (gennaio 2002): S61. http://dx.doi.org/10.1016/s0091-6749(02)81274-x.
Testo completo
36
Shinkai, Akeo, Hajime Yoshisue, Masamichi Koike, Emi Shoji, Satoshi Nakagawa, Akiko Saito, Tsuyoshi Takeda et al. "A Novel Human CC Chemokine, Eotaxin-3, Which Is Expressed in IL-4-Stimulated Vascular Endothelial Cells, Exhibits Potent Activity Toward Eosinophils". Journal of Immunology 163, n. 3 (1 agosto 1999): 1602–10. http://dx.doi.org/10.4049/jimmunol.163.3.1602.
Testo completoAbstract (sommario):
Abstract IL-4 has been shown to be involved in the accumulation of leukocytes, especially eosinophils, at sites of inflammation by acting on vascular endothelial cells. To identify novel molecules involved in the IL-4-dependent eosinophil extravasation, cDNA prepared from HUVEC stimulated with IL-4 was subjected to differential display analysis, which revealed a novel CC chemokine designated as eotaxin-3. The human eotaxin-3 gene has been localized to chromosome 7q11.2, unlike most other CC chemokine genes. The predicted mature protein of 71 aa showed 27–42% identity to other human CC chemokines. The recombinant protein induced a transient increase in the cytosolic Ca2+ concentration and in vitro chemotaxis on eosinophils. Furthermore, in cynomolgus monkeys, the accumulation of eosinophils was observed at the sites where the protein was injected. Eotaxin-3 inhibited the binding of 125I-eotaxin, but not 125I-macrophage inflammatory protein-1α, to eosinophils and acted on cell lines transfected with CCR-3, suggesting that eotaxin-3 recognized CCR-3. IL-13 as well as IL-4 up-regulated eotaxin-3 mRNA in HUVEC, whereas neither TNF-α, IL-1β, IFN-γ, nor TNF-α plus IFN-γ did. The expression profile of eotaxin-3 is different from those of eotaxin, RANTES, and monocyte chemoattractant protein-4, which are potent eosinophil-selective chemoattractants and are induced by either TNF-α or TNF-α plus IFN-γ. These results suggest that eotaxin-3 may contribute to the eosinophil accumulation in atopic diseases.
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Agrawal, Devendra, Min-Jung Kim e Rohit Gaurav. "Differential effects of TGF-β1 on IL-5 and eotaxin-induced chloride currents in human blood eosinophils (P5130)". Journal of Immunology 190, n. 1_Supplement (1 maggio 2013): 58.19. http://dx.doi.org/10.4049/jimmunol.190.supp.58.19.
Testo completoAbstract (sommario):
Abstract TGF-β1 is critical in the pathogenesis of chronic asthma and acts on eosinophils and other cells in the airways. Recently, we found TGF-β1 increases CLC3 expression in human blood eosinophils and induces migration. Here, we examined the interaction of TGF-β1 with IL-5 and eotaxin in the activation of chloride currents in human blood eosinophils. Eosinophils were purified (<99% pure, >98% viable) from the blood of healthy volunteers. Chloride current was measured at pH 7.4 by whole cell patch clamping in freshly isolated eosinophils using Axopatch 200B amplifier and analyzed by pClamp 10 software. Both eotaxin-1 and eotaxin-3 at low doses (0.075-10 ng/ml) increased outwardly rectified Cl- current in a time-dependent manner with maximum response at 500msec plus 100 mV. The eotaxin response at low doses (0.075-0.1 ng/ml) was slower in onset than at high dose. SB328437, a CCR3 antagonist (100 nM), inhibited eotaxin-induced Cl- current. Effect of eotaxin-3 was about 7-times larger than eotaxin-1. TGF-β1 (10ng/ml) decreased eotaxin-induced Cl- current. Incubation of eosinophils with IL-5 (10ng/ml) for 3hr decreased basal level of Cl- current. However, the addition of TGF-β1 with IL-5 significantly enhanced Cl- current. These data suggest differential effect of TGF-β1 in the activation and migration of human blood eosinophils in the presence of eotaxin or IL-5 in allergic airway inflammation and chronic asthma.
38
Yang, Yi, James Loy, Rolf-Peter Ryseck, Daniel Carrasco e Rodrigo Bravo. "Antigen-Induced Eosinophilic Lung Inflammation Develops in Mice Deficient in Chemokine Eotaxin". Blood 92, n. 10 (15 novembre 1998): 3912–23. http://dx.doi.org/10.1182/blood.v92.10.3912.
Testo completoAbstract (sommario):
Abstract The mechanisms that regulate the selective infiltration of eosinophils in certain allergic diseases are still poorly understood. The CC chemokine eotaxin is a potent chemoattractant, highly specific for eosinophils. Recent studies have implicated that eotaxin plays an important role in the recruitment of eosinophils in different inflammation processes. A number of other chemokines, cytokines, and chemoattractants also have chemotactic activities for eosinophils and some of them present high selectivity for eosinophils. To further study the role of eotaxin in inflammation, we generated mutant mice with the eotaxin gene disrupted and replaced by the Escherichia coliβ-galactosidase gene. These mice developed normally and had no histologic or hematopoietic abnormalities. Furthermore, our studies showed that the lack of eotaxin did not affect the recruitment of eosinophils in the inflammation models induced by Sephadex beads and thioglycollate, as well as in an experimental lung eosinophilia model induced by ovalbumin aerosol challenge, even at the onset of the inflammatory response. The replacement of the eotaxin gene by the β-galactosidase gene provided a useful marker to monitor the activity of the eotaxin promoter under normal conditions and after antigen challenges. Immunohistochemical staining suggested that endothelial cells were the major sources of eotaxin expression.
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Humbles, Alison A., Dolores M. Conroy, Sylvie Marleau, Sara M. Rankin, Roger T. Palframan, Amanda E. I. Proudfoot, Timothy N. C. Wells et al. "Kinetics of Eotaxin Generation and Its Relationship to Eosinophil Accumulation in Allergic Airways Disease: Analysis in a Guinea Pig Model In Vivo". Journal of Experimental Medicine 186, n. 4 (18 agosto 1997): 601–12. http://dx.doi.org/10.1084/jem.186.4.601.
Testo completoAbstract (sommario):
Challenge of the airways of sensitized guinea pigs with aerosolized ovalbumin resulted in an early phase of microvascular protein leakage and a delayed phase of eosinophil accumulation in the airway lumen, as measured using bronchoalveolar lavage (BAL). Immunoreactive eotaxin levels rose in airway tissue and BAL fluid to a peak at 6 h falling to low levels by 12 h. Eosinophil numbers in the tissue correlated with eotaxin levels until 6 h but eosinophils persisted until the last measurement time point at 24 h. In contrast, few eosinophils appeared in BAL over the first 12 h, major trafficking through the airway epithelium occurring at 12–24 h when eotaxin levels were low. Constitutive eotaxin was present in BAL fluid. Both constitutive and allergen-induced eosinophil chemoattractant activity in BAL fluid was neutralized by an antibody to eotaxin. Allergen-induced eotaxin appeared to be mainly in airway epithelium and macrophages, as detected by immunostaining. Allergen challenge of the lung resulted in a rapid release of bone marrow eosinophils into the blood. An antibody to IL-5 suppressed bone marrow eosinophil release and lung eosinophilia, without affecting lung eotaxin levels. Thus, IL-5 and eotaxin appear to cooperate in mediating a rapid transfer of eosinophils from the bone marrow to the lung in response to allergen challenge.
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Wang, Wen, Ci-You Huang, Zhuo-Ping Wang, Shan-Shan Xu, Tie-Yong Qian, Yi-Ding Chen e Wei-Guo Wu. "Serum C-C motif ligand 11/eotaxin-1 may serve as a candidate biomarker for postmenopausal osteoporosis". Journal of Medical Biochemistry 38, n. 3 (11 maggio 2019): 353–60. http://dx.doi.org/10.2478/jomb-2018-0042.
Testo completoAbstract (sommario):
Summary Background The chemokine C-C motif ligand 11, also known as eotaxin-1, has been identified as a novel mediator of inflammatory bone resorption. However, little is known regarding a potential role for CCL11/Eotaxin-1 in postmenopausal osteoporosis. Objective The scope of this study was to explore the relationship between serum CCL11/Eotaxin-1 concentrations and disease progression of postmenopausal females with osteoporosis. Methods A total of 83 postmenopausal women diagnosed with osteoporosis were enrolled. Meanwhile, 82 postmenopausal women with normal bone mineral density (BMD) and 85 healthy controls inner child-bearing age were enrolled as control. The Dual-energy X-ray absorptiometry was used to examine the BMDs at the femoral neck, lumbar spine 1-4 and total hip of all participants. Serum CCL11/Eotaxin-1 levels were examined by enzyme-linked immunosorbent assay. We also included inflammation marker interleukin-6 (IL-6) as well as a serum marker of bone resorption C-telopeptide cross-linked collagen type 1 (CTX-1). The Visual Analogue Scale (VAS) and Oswestry Disability Index (ODI) were recorded to evaluate the clinical severity in POMP females. Results Serum CCL11/Eotaxin-1 levels were significantly elevated in postmenopausal osteoporotic patients PMOP patients compared with PMNOP and healthy controls. We observed a significant negative correlation of serum CCL11/Eotaxin-1 levels with lumbar spine, femoral neck and total hip BMD. Furthermore, serum CCL11/ Eotaxin-1 concentrations were also positively related to the VAS and ODI scores. Last, serum CCL11/ Eotaxin-1 concentrations were positively associated with IL-6 and CTX-1 levels. These correlations remain significant after adjusting for age and BMI. Multivariate linear regression analysis demonstrated that CCL11/Eotaxin-1 could serve as an independent marker. Conclusions Serum CCL 11/Eotaxin-1 may serve as a candidate biomarker for postmenopausal osteoporosis. Therapeutics targeting CCL11/Eotaxin-1 and its related signalling way to prevent and slow progression of PMOP deserve further study.
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Moore, Paul E., Trudi L. Church, David D. Chism, Reynold A. Panettieri e Stephanie A. Shore. "IL-13 and IL-4 cause eotaxin release in human airway smooth muscle cells: a role for ERK". American Journal of Physiology-Lung Cellular and Molecular Physiology 282, n. 4 (1 aprile 2002): L847—L853. http://dx.doi.org/10.1152/ajplung.00245.2001.
Testo completoAbstract (sommario):
Human airway smooth muscle (HASM) cells express interleukin (IL)-13 and IL-4 receptors and respond to these cytokines with signal transducer and activator of transcription-6 and extracellular signal-regulated kinase (ERK) activation. The purpose of this study was to determine whether IL-13 and/or IL-4 influence eotaxin release in HASM cells and whether the ERK mitogen-activated protein (MAP) kinase pathway is involved in these events. Eotaxin release into HASM cell supernatants was assayed by ELISA, and eotaxin mRNA expression was determined by Northern blot analysis. Pretreatment with either IL-13 or IL-4 resulted in a concentration- and time-dependent release of eotaxin, although IL-4 was more effective. Eotaxin release was approximately twice baseline after treatment with 50 ng/ml IL-13 or IL-4 ( P < 0.001). IL-13 and IL-4 also acted synergistically with tumor necrosis factor (TNF)-α to induce eotaxin release: TNF-α alone (10 ng/ml for 24 h) resulted in an approximately fourfold increase in eotaxin release, whereas TNF-α in combination with IL-13 or IL-4 resulted in 10- or 20-fold increases ( P < 0.05). Similar results were obtained for eotaxin mRNA expression. Pretreatment with either U-0126 (10 μM) or PD-98059 (30 μM), both inhibitors of MAP/ERK kinase, the enzyme upstream of ERK, inhibited IL-13- or IL-4-induced eotaxin release ( P < 0.05). U-0126 also inhibited IL-13, and TNF-α induced mRNA expression. Our results indicate that IL-13 and IL-4 cause eotaxin release in HASM cells through a mechanism that, in part, involves ERK activation and suggest that the smooth muscle may be an important source of chemokines leading to eosinophil recruitment in asthma.
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Furer, Victoria, Eyal Hazan, Adi Mor, Michal Segal, Avi Katav, Valerie Aloush, Ori Elkayam, Jacob George e Jacob N. Ablin. "Elevated Levels of Eotaxin-2 in Serum of Fibromyalgia Patients". Pain Research and Management 2018 (2018): 1–4. http://dx.doi.org/10.1155/2018/7257681.
Testo completoAbstract (sommario):
FMS patients demonstrate an altered profile of chemokines relative to healthy controls (HC). Eotaxin-2 is a potent chemoattractant distributed in a variety of tissues. The aim of the study was to compare serum levels of eotaxin-2 between FMS patients and HC and to examine a potential correlation between eotaxin-2 levels and clinical parameters of FMS. Methods. 50 patients with FMS and 15 HC were recruited. Data on the severity of FMS symptoms and depression were collected. Serum levels of eotaxin-2 (ELISA) were determined in all participants. High-sensitive CRP (hs-CRP) was measured in the FMS group. Results. The FMS cohort included predominantly females (84%), mean age of 49, and mean disease duration of 6 years. FMS patients exhibited significantly higher eotaxin-2 levels (pg/ml) versus HC: 833 (±384) versus 622 (±149), p=0.04. Mean hs-CRP level among FMS patients was 4.8 ± 6 mg/l, a value not indicative of acute inflammation. No correlation was found between eotaxin-2 and hs-CRP levels. No correlation was found between eotaxin-2 and severity measures of FMS or depression. Conclusion. Eotaxin-2 does not appear to be a candidate for a disease activity biomarker in FMS. Further research is warranted into the role of this chemokine in the pathophysiology of the FMS.
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Nakamura, Hidetoshi, Kathleen J. Haley, Toshiko Nakamura, Andrew D. Luster e Craig M. Lilly. "Differential regulation of eotaxin expression by TNF-α and PMA in human monocytic U-937 cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 275, n. 3 (1 settembre 1998): L601—L610. http://dx.doi.org/10.1152/ajplung.1998.275.3.l601.
Testo completoAbstract (sommario):
Regulation of eotaxin expression was investigated in U-937 cells, a human monocyte-like cell line. Eotaxin mRNA was induced by tumor necrosis factor-α (TNF-α; 0.1–100 ng/ml) and phorbol 12-myristate 13-acetate (PMA; 0.01–1 μM). PMA-induced eotaxin mRNA expression was of greater magnitude and was maximal at a later time point than TNF-α-induced expression (16 h vs. 2 h after stimulation), which was consistent with eotaxin protein expression detected by immunocytochemistry. Dexamethasone (0.01–10 μM) decreased eotaxin mRNA expression in both TNF-α- and PMA-stimulated U-937 cells. PMA-induced eotaxin mRNA expression was inhibited by cycloheximide (10 μg/ml), whereas TNF-α-induced expression was not. The protein kinase C (PKC) inhibitor staurosporine (10–50 nM) inhibited PMA-induced eotaxin mRNA expression, whereas TNF-α-induced expression was enhanced by this reagent. These results suggest that eotaxin expression can be induced by more than one mechanism: the PMA-triggered pathway is mediated by PKC activation and requires new protein synthesis, whereas the TNF-α-triggered pathway is independent of PKC and protein synthesis. TNF-α- and PMA-induced pathways are both associated with nuclear factor-κB, because its binding activity was enhanced in the presence of these stimuli, and both pathways were limited by its inhibitor, diethyldithiocarbamate.
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Lamkhioued, B., P. M. Renzi, S. Abi-Younes, E. A. Garcia-Zepada, Z. Allakhverdi, O. Ghaffar, M. D. Rothenberg, A. D. Luster e Q. Hamid. "Increased expression of eotaxin in bronchoalveolar lavage and airways of asthmatics contributes to the chemotaxis of eosinophils to the site of inflammation." Journal of Immunology 159, n. 9 (1 novembre 1997): 4593–601. http://dx.doi.org/10.4049/jimmunol.159.9.4593.
Testo completoAbstract (sommario):
Abstract Presently, there is considerable evidence for the participation of eosinophils in the pathophysiology of human bronchial asthma. Although increased numbers of eosinophils are present in the airways and bronchoalveolar lavage (BAL) fluid of atopic asthmatics, the mechanisms responsible for their preferential accumulation are still largely unknown. Eotaxin is a chemokine that promotes the selective recruitment of eosinophils. We report that atopic asthmatic patients have high concentrations of eotaxin in BAL fluid and an increased expression of eotaxin mRNA and protein in the epithelium and submucosa of their airways when compared with normal controls. In the BAL cells from asthmatic patients, eotaxin immunoreactivity colocalized predominantly to macrophages (62.2%), with a lesser contribution from T cells (16.3%) and eosinophils (8.9%). BAL fluid from asthmatics contained chemotactic activity for eosinophils that was attributable in part to the presence of eotaxin. Moreover, eotaxin was more effective at inducing in vitro eosinophil chemotaxis when eosinophils were stimulated with IL-5 (a cytokine that enhances the effector capacity of mature eosinophils). These observations suggest that eotaxin contributes to the pathogenesis of asthma by the specific recruitment of eosinophils into the airways.
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Peled, Amnon, Jose Angel Gonzalo, Clare Lloyd e Jose-Carlos Gutierrez-Ramos. "The Chemotactic Cytokine Eotaxin Acts as a Granulocyte-Macrophage Colony-Stimulating Factor During Lung Inflammation". Blood 91, n. 6 (15 marzo 1998): 1909–16. http://dx.doi.org/10.1182/blood.v91.6.1909.
Testo completoAbstract (sommario):
Abstract During inflammatory processes, inflamed tissues signal the bone marrow (BM) to produce more mature leukocytes in ways that are not yet understood. We report here that, during the development of lung allergic inflammation, the administration of neutralizing antibodies to the chemotactic cytokine, Eotaxin, prevented the increase in the number of myeloid progenitors produced in the BM, therefore reducing the output of mature myeloid cells from BM. Conversely, the in vivo administration of Eotaxin increased the number of myeloid progenitors present in the BM. Furthermore, we found that, in vitro, Eotaxin is a colony-stimulating factor for granulocytes and macrophages. Eotaxin activity synergized with stem cell factor but not with interleukin-3 or granulocyte-macrophage colony-stimulating factor and was inhibited bypertussis toxin. We report also that CCR-3, the receptor for Eotaxin, was expressed by hematopoietic progenitors (HP). Thus, during inflammation, Eotaxin acts in a paracrine way to shift the differentiation of BM HP towards the myeloid lineage.
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Peled, Amnon, Jose Angel Gonzalo, Clare Lloyd e Jose-Carlos Gutierrez-Ramos. "The Chemotactic Cytokine Eotaxin Acts as a Granulocyte-Macrophage Colony-Stimulating Factor During Lung Inflammation". Blood 91, n. 6 (15 marzo 1998): 1909–16. http://dx.doi.org/10.1182/blood.v91.6.1909.1909_1909_1916.
Testo completoAbstract (sommario):
During inflammatory processes, inflamed tissues signal the bone marrow (BM) to produce more mature leukocytes in ways that are not yet understood. We report here that, during the development of lung allergic inflammation, the administration of neutralizing antibodies to the chemotactic cytokine, Eotaxin, prevented the increase in the number of myeloid progenitors produced in the BM, therefore reducing the output of mature myeloid cells from BM. Conversely, the in vivo administration of Eotaxin increased the number of myeloid progenitors present in the BM. Furthermore, we found that, in vitro, Eotaxin is a colony-stimulating factor for granulocytes and macrophages. Eotaxin activity synergized with stem cell factor but not with interleukin-3 or granulocyte-macrophage colony-stimulating factor and was inhibited bypertussis toxin. We report also that CCR-3, the receptor for Eotaxin, was expressed by hematopoietic progenitors (HP). Thus, during inflammation, Eotaxin acts in a paracrine way to shift the differentiation of BM HP towards the myeloid lineage.
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Nie, Mingrong, Qingxiang Zeng, Luo Xi, Yiquan Tang, Renzhong Luo e Wenlong Liu. "The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines". Mediators of Inflammation 2021 (3 dicembre 2021): 1–7. http://dx.doi.org/10.1155/2021/1110671.
Testo completoAbstract (sommario):
Background. Airway epithelium plays an important role during the development of allergic rhinitis (AR), which is characterized by production of thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25). IL-35, mainly expressed by Treg cells, have negative regulation in Th2, Th17, and ILC2 inflammation. However, the effect of IL-35 on human nasal epithelial cells (HNECs) especially the secretion of nasal epithelial-derived proinflammatory cytokines as well as the possible mechanism is still unclear. Methods. HNECs were cultured and stimulated by various stimulators. The expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 from supernatant was measured using real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). AR mice were developed to verify the effect of IL-35 on nasal epithelial cells in vivo. Results. After Poly I:C stimulation, IL-35 inhibited the production of IL-25, and TSLP from HNECs increased significantly compared with baseline levels ( P < 0.05 ). After Dermatophagoides pteronyssinus or Aspergillus fumigatus stimulation, IL-35 inhibited the production of IL-25, IL-33, and TSLP from HNECs increased significantly compared with baseline levels ( P < 0.05 ). After Dermatophagoides pteronyssinus, IL-35 inhibited the production of eotaxin-1, eotaxin-2, and eotaxin-3 released from HNECs increased significantly compared with baseline levels ( P < 0.05 ). Similarly, IL-35-treated AR mice presented with decreased expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 in nasal lavage fluid. Conclusion. IL-35 suppressed both type 2 inflammation-inducing cytokines and eosinophil chemotactic factor from HNECs, suggesting the important role of IL-35 during the development of AR.
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Takamura, Kei, Yasuyuki Nasuhara, Motoko Kobayashi, Tomoko Betsuyaku, Yoko Tanino, Ichiro Kinoshita, Etsuro Yamaguchi, Satoshi Matsukura, Robert P. Schleimer e Masaharu Nishimura. "Retinoic acid inhibits interleukin-4-induced eotaxin production in a human bronchial epithelial cell line". American Journal of Physiology-Lung Cellular and Molecular Physiology 286, n. 4 (aprile 2004): L777—L785. http://dx.doi.org/10.1152/ajplung.00289.2003.
Testo completoAbstract (sommario):
Retinoic acid (RA) is known to accelerate wound healing and induce cell differentiation. All- trans RA (ATRA) exerts its effect by binding retinoic acid receptors, which are members of the nuclear receptor family. We investigated whether RA can alter expression of eotaxin, a potent eosinophil chemoattractant that is regulated by the transcription factors signal transducer and activator of transcription 6 (STAT6) and NF-κB. We examined the effects of RA on eotaxin expression in a human bronchial epithelial cell line BEAS-2B. ATRA and its stereodimer 9- cis retinoic acid (9- cis RA) inhibited IL-4-induced release of eotaxin at 10-6M by 78.0 and 52.0%, respectively ( P < 0.05). ATRA and 9- cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10-6M by 52.3 and 53.5%, respectively ( P < 0.05). In contrast, neither ATRA nor 9- cis RA had any effects on TNF-α-induced eotaxin production. In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Interestingly, ATRA had no effects on IL-4-induced tyrosine phosphorylation, nuclear translocation, or DNA binding activity of STAT6. Activating protein-1 was not involved in ATRA-mediated transrepression of eotaxin with IL-4 stimulation. The mechanism of the inhibitory effect of ATRA on IL-4-induced eotaxin production in human bronchial epithelial cells has not been elucidated but does not appear to be due to an effect on STAT6 activation. These findings raise the possibility that RA may reduce eosinophilic airway inflammation, one of the prominent pathological features of allergic diseases such as bronchial asthma.
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Palframan, Roger T., Paul D. Collins, Timothy J. Williams e Sara M. Rankin. "Eotaxin Induces a Rapid Release of Eosinophils and Their Progenitors From the Bone Marrow". Blood 91, n. 7 (1 aprile 1998): 2240–48. http://dx.doi.org/10.1182/blood.v91.7.2240.
Testo completoAbstract (sommario):
Abstract The CC-chemokine eotaxin is a potent eosinophil chemoattractant that stimulates recruitment of eosinophils from the blood to sites of allergic inflammation. Mobilization from the bone marrow is an important early step in eosinophil trafficking during the allergic inflammatory response. In this paper we examine the potential of eotaxin to mobilize eosinophils and their progenitors from bone marrow. Eotaxin stimulated selective, dose-dependent chemotaxis of guinea pig bone marrow eosinophils in vitro. Intravenous injection of eotaxin (1 nmol/kg) into guinea pigs in vivo stimulated a rapid blood eosinophilia (from 3.9 ± 1.2 to 28 ± 9.9 × 104eosinophils/mL at 30 minutes) and a corresponding decrease in the number of eosinophils retained in the femoral marrow (from 9.0 ± 0.8 to 4.8 ± 0.8 × 106 eosinophils per femur). To show a direct release of eosinophils from the bone marrow an in situ perfusion system of the guinea pig femoral bone marrow was developed. Infusion of eotaxin into the arterial supply of the perfused femoral marrow stimulated a rapid and selective release of eosinophils into the draining vein. In addition, eotaxin stimulated the release of colony-forming progenitor cells. The cytokine interleukin-5 was chemokinetic for bone marrow eosinophils and exhibited a marked synergism with eotaxin with respect to mobilization of mature eosinophils from the femoral marrow. Thus, eotaxin may be involved in both the mobilization of eosinophils and their progenitors from the bone marrow into the blood and in their subsequent recruitment into sites of allergic inflammation.
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Palframan, Roger T., Paul D. Collins, Timothy J. Williams e Sara M. Rankin. "Eotaxin Induces a Rapid Release of Eosinophils and Their Progenitors From the Bone Marrow". Blood 91, n. 7 (1 aprile 1998): 2240–48. http://dx.doi.org/10.1182/blood.v91.7.2240.2240_2240_2248.
Testo completoAbstract (sommario):
The CC-chemokine eotaxin is a potent eosinophil chemoattractant that stimulates recruitment of eosinophils from the blood to sites of allergic inflammation. Mobilization from the bone marrow is an important early step in eosinophil trafficking during the allergic inflammatory response. In this paper we examine the potential of eotaxin to mobilize eosinophils and their progenitors from bone marrow. Eotaxin stimulated selective, dose-dependent chemotaxis of guinea pig bone marrow eosinophils in vitro. Intravenous injection of eotaxin (1 nmol/kg) into guinea pigs in vivo stimulated a rapid blood eosinophilia (from 3.9 ± 1.2 to 28 ± 9.9 × 104eosinophils/mL at 30 minutes) and a corresponding decrease in the number of eosinophils retained in the femoral marrow (from 9.0 ± 0.8 to 4.8 ± 0.8 × 106 eosinophils per femur). To show a direct release of eosinophils from the bone marrow an in situ perfusion system of the guinea pig femoral bone marrow was developed. Infusion of eotaxin into the arterial supply of the perfused femoral marrow stimulated a rapid and selective release of eosinophils into the draining vein. In addition, eotaxin stimulated the release of colony-forming progenitor cells. The cytokine interleukin-5 was chemokinetic for bone marrow eosinophils and exhibited a marked synergism with eotaxin with respect to mobilization of mature eosinophils from the femoral marrow. Thus, eotaxin may be involved in both the mobilization of eosinophils and their progenitors from the bone marrow into the blood and in their subsequent recruitment into sites of allergic inflammation.