Relevant bibliographies by topics / Phagocytic cell

Academic literature on the topic 'Phagocytic cell'

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Published: 11 March 2023

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Journal articles on the topic "Phagocytic cell"

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Bondarenko, L. "The cell protection of weated pigs for probiotics." Tehnologìâ virobnictva ì pererobki produktìv tvarinnictva, no. 2(158) (November 24, 2020): 111–19. http://dx.doi.org/10.33245/2310-9289-2020-158-2-111-119.

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The immune system is central to ensuring the consistency of the body's homeostasis. The state of the body's natural resistance is determined by a set of non-specific protective mechanisms. Lymphocytes and phagocytes are actively involved in maintaining immunity. Lymphocytes recognize the antigens of pathogenic microorganisms, and phagocytes absorb and destroy the pathogens themselves. During the weaning of piglets from sows there is a decrease in the protective forces of their body. During this period, the natural resistance of the piglets is reduced due to the stressful situation caused by changing conditions of confinement, the transition to full feed and lack of sows. The immune system of weaning pigs is relatively weak, so when exposed to environmental and technological stressors, they become susceptible to various diseases. The use of probiotic drugs stimulates the activity of the immune system, prevents stress and immunodeficiency. One of these probiotics is the probiotic of domestic production Protecto-active. It w observed the the influence of the probiotic Protecto-active on the indices of nonspecific resistance of the young pigs organism to the growth. An increase in bactericidal activity of blood serum by 12.10% (P <0.05) and lysozyme activity of blood in the piglets of the experimental group was increased by 3.71% compared to control, which indicates the activation of the body's defenses and the increase in adaptive capacity. An important step in the study of the influence of the probiotic Protekto-active on the state of the immune system is to determine the phagocytic activity of neutrophils, phagocytic index and phagocytic number. In the experimental group of piglets that were fed the probiotic Protecto-active, we found an increase in leukocyte phagocytic activity by 9.0% (P <0.001), a phagocytic index by 51.7% (P<0.001) and a phagocytic number by 24.8% ( P <0.01) compared with the control group. Thus, using a probiotic Protecto-active, all indicators of phagocytosis increase: the number of phagocytes increases, their ability to capture microorganisms and increases their digestive capacity, it increases the bacterial and lysozyme activity of blood serum, which is positively reflected in the immunobiosity. Key words: probiotic, phagocytosis, phagocytic index, phagocytic number, phagocytic activity of leukocytes, cellular immunity, piglets
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Jiang, Shuai, Zhihao Jia, Tao Zhang, Lingling Wang, Limei Qiu, Jinsheng Sun, and Linsheng Song. "Functional characterisation of phagocytes in the Pacific oyster Crassostrea gigas." PeerJ 4 (December 14, 2016): e2590. http://dx.doi.org/10.7717/peerj.2590.

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Invertebrates lack canonical adaptive immunity and mainly rely on innate immune system to fight against pathogens. The phagocytes, which could engulf and kill microbial pathogens, are likely to be of great importance and have to undertake significant roles in invertebrate immune defense. In the present study, flow cytometry combined with histological and lectin staining was employed to characterise functional features of phagocytes in the Pacific oyster Crassostrea gigas. Based on the cell size and cellular contents, haemocytes were categorised into three cell types, i.e., granulocytes, semigranulocytes and agranulocytes. Agranulocytes with smaller cell volume and lower cytoplasmic-to-nuclear ratio did not show phagocytic activity, while semigranulocytes and agranulocytes exhibited larger cell volume, higher cytoplasmic-to-nuclear ratio and phagocytic activity. In addition, granulocytes with higher side scatter (SSC) exhibited higher phagocytic activity than that of semigranulocytes. When β-integrin and lectin-like receptors were blocked by RGD tripeptide and carbohydrates, respectively, the phagocytic activity of both granulocytes and semigranulocytes was significantly inhibited, indicating that β-integrin and certain lectin-like receptors were involved in phagocytosis towards microbes. Moreover, lipopolysaccharide but not peptidylglycan could enhance phagocytic activity of granulocytes and semigranulocytes towards Vibrio splendidus and Staphylococcus aureus. Lectin staining analysis revealed that Lycopersicon esculentum lectin (LEL), binding the epitope polylactosamine, was highly distributed on the extracellular cell surface of phagocytes, and could be utilized as a potential molecular marker to differentiate phagocytes from non-phagocytic haemocytes. The results, collectively, provide knowledge on the functional characters of oyster phagocytes, which would contribute to deep investigation of cell typing and cellular immunity in bivalves.
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QUIE, P. "Phagocytic cell dysfunction." Journal of Allergy and Clinical Immunology 77, no. 3 (March 1986): 387–98. http://dx.doi.org/10.1016/0091-6749(86)90169-7.

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Tussupbekova, Gulmira, Anar Rakhmetova, Gulnaziya Alshynbekova, Ryszhan Bakirova, Y. Kuandykov, Madina Molsadykkyzy, Balgyn Amanbay, Asan Gulmira Kudaibergenkyzy, Aizhan Beisenova, and Aizhan Moldakaryzova. "Influence of Industrial Factors on Cytomorphological Indicators of Phagocytic Cells." Open Access Macedonian Journal of Medical Sciences 10, A (June 30, 2022): 1207–10. http://dx.doi.org/10.3889/oamjms.2022.5939.

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AIM: The article has researched cell morphological changes of phagocytic system’s cell of experimented animals by influence of cool-rock dust phisical loading basis. METHODS: The phagocytic activity in combined operation of destructive changes in the cells and the lowering of vital capacity was investigated. RESULTS: The taken results let cosider the structure-functional condition of the phagocytal system’s cell in operation of unfavorable and industrial factors. CONCLUSION: Experimental animals with intratracheal administration of CRD have pronounced changes in phagocytic activity in AML, RBM and PA as compared with the control group.
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Lovewell, Rustin R., Sandra M. Hayes, George A. O'Toole, and Brent Berwin. "Pseudomonas aeruginosaflagellar motility activates the phagocyte PI3K/Akt pathway to induce phagocytic engulfment." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 7 (April 1, 2014): L698—L707. http://dx.doi.org/10.1152/ajplung.00319.2013.

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Phagocytosis of the bacterial pathogen Pseudomonas aeruginosa is the primary means by which the host controls bacterially induced pneumonia during lung infection. Previous studies have identified flagellar swimming motility as a key pathogen-associated molecular pattern (PAMP) recognized by phagocytes to initiate engulfment. Correspondingly, loss of flagellar motility is observed during chronic pulmonary infection with P. aeruginosa, and this likely reflects a selection for bacteria resistant to phagocytic clearance. However, the mechanism underlying the preferential phagocytic response to motile bacteria is unknown. Here we have identified a cellular signaling pathway in alveolar macrophages and other phagocytes that is specifically activated by flagellar motility. Genetic and biochemical methods were employed to identify that phagocyte PI3K/Akt activation is required for bacterial uptake and, importantly, it is specifically activated in response to P. aeruginosa flagellar motility. Based on these observations, the second important finding that emerged from these studies is that titration of the bacterial flagellar motility results in a proportional activation state of Akt. Therefore, the Akt pathway is responsive to, and corresponds with, the degree of bacterial flagellar motility, is independent of the actin polymerization that facilitates phagocytosis, and determines the phagocytic fate of P. aeruginosa. These findings elucidate the mechanism behind motility-dependent phagocytosis of extracellular bacteria and support a model whereby phagocytic clearance exerts a selective pressure on P. aeruginosa populations in vivo, which contributes to changes in pathogenesis during infections.
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Holzer, T. J., L. Kizlaitis, M. Vachula, C. W. Weaver, and B. R. Andersen. "Human phagocytic cell responses to Mycobacterium leprae and Mycobacterium bovis Bacillus Calmette-Guérin. An in vitro comparison of leprosy vaccine components." Journal of Immunology 141, no. 5 (September 1, 1988): 1701–8. http://dx.doi.org/10.4049/jimmunol.141.5.1701.

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Abstract Components of current vaccines for Hansen's disease include Mycobacterium bovis Bacillus Calmette-Guérin (BCG) and killed Mycobacterium leprae. BCG infections in humans are rare and most often occur in immune-compromised individuals. M. leprae on the other hand, although not causing clinical disease in most exposed individuals, is capable of infecting and replicating within mononuclear phagocytes. Lymphocytes from patients with the lepromatous form of Hansen's disease exhibit defective lymphokine production when challenged in vitro with M. leprae. This may result in inefficient mononuclear phagocyte activation for oxidative killing. To study the ability of normal phagocytes to ingest and respond oxidatively to BCG and M. leprae, we measured phagocytic cell O2- release and fluorescent oxidative product formation and visually confirmed the ingestion of the organisms. BCG stimulated a vigorous O2- generation in neutrophils and monocytes and flow cytometric oxidative product generation by neutrophils occurred in the majority of cells. M. leprae, stimulated a weak but significant O2- release requiring a high concentration of organisms and long exposure. By flow cytometric analysis, most neutrophils were able to respond to both organisms with the generation of fluorescent oxidative products. Neutrophil oxidative responses to M. leprae were substantially less than responses seen from neutrophils exposed to BCG. By microscopic examination of neutrophils phagocytizing FITC-labeled bacteria, it was shown that both M. leprae and BCG were slowly ingested but that more BCG appeared to be associated with the cell membrane of more of the cells. When phagocytic cells were incubated with BCG and M. leprae for 30 min and subsequently examined by electron microscopy, few organisms were seen in either neutrophils or monocytes. This suggests that BCG are easily recognized and slowly ingested by normal phagocytic cells, the majority of which respond with a strong oxidative burst. M. leprae appeared to only weakly stimulate phagocyte oxidative responses and were also slowly phagocytized.
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Snipes, RG, KW Lam, RC Dodd, TK Gray, and MS Cohen. "Acid phosphatase activity in mononuclear phagocytes and the U937 cell line: monocyte-derived macrophages express tartrate-resistant acid phosphatase." Blood 67, no. 3 (March 1, 1986): 729–34. http://dx.doi.org/10.1182/blood.v67.3.729.729.

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Abstract Tartrate-resistant acid phosphatase (TRAcP) is used as a marker for osteoclasts, which are believed to be derived from phagocytic cells or phagocyte stem cell precursors. To further investigate the relationship between monocytic phagocytes and osteoclasts, acid phosphatase (AcP) activity was measured by three different techniques in human peripheral blood monocytes, monocyte-derived macrophages, and the U937 cell line. We found that cytochemistry and gel electrophoresis led to similar results, but that the colorimetric assay was inconsistent. Normal human peripheral monocytes expressed both tartrate-sensitive and -resistant AcP. In culture these cells formed polykaryons and expressed TRAcP activity that was further identified as an isoenzyme associated with bone tissue. In contrast, the U937 cells did not express TRAcP activity as measured by gel electrophoresis. Both U937 cells and monocytes possess material that interferes with interpretation of the colorimetric assay of AcP. The presence of TRAcP in monocyte-derived macrophages further supports the relationship between phagocytic cells and bone osteoclasts.
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Snipes, RG, KW Lam, RC Dodd, TK Gray, and MS Cohen. "Acid phosphatase activity in mononuclear phagocytes and the U937 cell line: monocyte-derived macrophages express tartrate-resistant acid phosphatase." Blood 67, no. 3 (March 1, 1986): 729–34. http://dx.doi.org/10.1182/blood.v67.3.729.bloodjournal673729.

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Tartrate-resistant acid phosphatase (TRAcP) is used as a marker for osteoclasts, which are believed to be derived from phagocytic cells or phagocyte stem cell precursors. To further investigate the relationship between monocytic phagocytes and osteoclasts, acid phosphatase (AcP) activity was measured by three different techniques in human peripheral blood monocytes, monocyte-derived macrophages, and the U937 cell line. We found that cytochemistry and gel electrophoresis led to similar results, but that the colorimetric assay was inconsistent. Normal human peripheral monocytes expressed both tartrate-sensitive and -resistant AcP. In culture these cells formed polykaryons and expressed TRAcP activity that was further identified as an isoenzyme associated with bone tissue. In contrast, the U937 cells did not express TRAcP activity as measured by gel electrophoresis. Both U937 cells and monocytes possess material that interferes with interpretation of the colorimetric assay of AcP. The presence of TRAcP in monocyte-derived macrophages further supports the relationship between phagocytic cells and bone osteoclasts.
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Wilson, M. E., R. J. Genco, and R. Snyderman. "The Phagocytic Cell: Summary." Clinical Infectious Diseases 7, no. 3 (May 1, 1985): 387–89. http://dx.doi.org/10.1093/clinids/7.3.387.

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Verhoef, J., and F. A. Waldvogel. "Testing phagocytic cell function." European Journal of Clinical Microbiology 4, no. 4 (August 1985): 379–81. http://dx.doi.org/10.1007/bf02148686.

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Dissertations / Theses on the topic "Phagocytic cell"

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Chao, D. "The role of the accessory cell in the immune response." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382569.

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Pound, J. D. "Parameters of human macrophage activation." Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381442.

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Maslen, Christina Louise. "The effects of anti-inflammatory compounds on the oxidative metabolism of human phagocytic cells." Thesis, University of Bath, 1985. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.353398.

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Phagocytic cells respond to activation by a variety of stimuli by generating oxygen-derived free radicals. The characteristics of the production of superoxide anion and hydrogen peroxide by human neutrophils has been compared with that produced by human monocytes. The majority of work in this thesis is concerned with the employment of an assay which measures hydrogen peroxide produced by stimulated human neutrophils in vitro, but which also has been found to detect the generation of another peroxide, the identity of which is uncertain. The use of cyclooxygenase, lipoxygenase and phospholipase A2 pathway inhibitors has provided indirect evidence for the identification of the unknown peroxide as 5-hydroperoxyeicosatetraenoic acid (5-HPETE). These inhibitors have also provided the opportunity to investigate differences in the oxidative metabolism of human neutrophils induced by various stimuli. In addition, the effects of two cyclooxygenase inhibitors, diclofenac and piroxicam, on neutrophil activity in vivo has been investigated. Whilst neutrophil activity of some individuals was inhibited, this was not consistent and not significant. Incubation of a variety of analogues of the cyclooxygenase inhibitors diclofenac and fenclofenac with stimulated neutrophils in vitro has allowed an insight into the structure-activity relationships of these drugs' effects on neutrophil activity. It was found that the position of substitution of various groups in the ring structure remote from the acid group had the biggest single influence on activity. Finally, the oxidative metabolism of neutrophils from patients with progressive systemic sclerosis, rheumatoid arthritis and peripheral vascular disease has been compared with that of neutrophils from healthy controls. The neutrophils from the progressive systemic sclerosis group were found to have increased activity both ex vivo and following incubation with heat-aggregated IgG. This has been shown to be associated with enhanced expression of Fc receptors on these cells.
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Uszak-Woronowicz, Alicja. "Trypanosoma cruzi, study on parasite culture conditions and non-phagocytic host cell interaction." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63381.pdf.

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Johnson, E. M. "In vitro effects of antifungal drugs on Candida albicans and phagocytic cell function." Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375031.

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Gibson, Joanne. "Characterisation of the differential phagocytic, cytokine and T cell activation potentials of bone marrow derived dendritic cells in response to C.albincans cell wall glycosylation." Thesis, University of Aberdeen, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542629.

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This thesis study investigated the involvement of glycosylation of cell wall proteins, major components of the outermost cell wall layer of C. albicans, in the induction of murine bone marrow derived dendritic cell (BMDC) responses. Utilising mutants which are deficient in glycosylation process, the binding of specific N-glycosylation moieties was demonstrated to be important in triggering phagocytosis while changes in O-glycosylation moieties altered the secretion of multiple pro-inflammatory chemokines and cytokines. Importantly, BMDC-O-glycosylation and/or BMDC-inner cell wall constituent interactions were demonstrated to result in the modulation of T cell responses, through the stimulation of the secretion of interleukin (IL)-17. It was further shown using receptor-deficient BMDC and receptor-blocking antibodies that although dectin-1, mannose receptor (MR) and Toll-like receptor (TLR)4 do not play a role in the induction of phagocytosis, receptor engagement induced receptor-specific cytokine secretion. Specifically, the secretion of IL-12p70 and IL-6 was dependent on dectin-1 signalling, while the secretion of the pro-inflammatory monocyte chemotactic protein (MCP)-1, tumour necrosis factor (TNF)-α and IL-6 were found to be induced in a MR-dependent manner. Intriguingly, a redundant role was found for TLR4. Cumulatively these results indicate a critical role of the recognition of fungal cell wall glycosylation moieties in the induction of protective phagocytosis and cytokine response in BMDC. Future studies to determine the role of other lectin receptors such as dectin-2 or receptor combinations will provide further insights into the complex interactions between BMDC and C. albicans.
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Blomgran, Robert. "Microbe-induced apoptosis in phagocytic cells and its role in innate immunity." Doctoral thesis, Linköping : Linköping University, 2006. http://www.bibl.liu.se/liupubl/disp/disp2006/med956s.pdf.

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Tolentino, Timothy P. "The Roles of Membrane Rafts in CD32A Mediated Formation of a Phagocytic Contact Area." Diss., Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/16127.

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Membrane rafts are highly dynamic heterogeneous sterol- and sphingolipid-rich micro-domains on cell surfaces. They are generally believed to provide residency for cell surface molecules (e.g., adhesion and signaling molecules) and scaffolding to facilitate the functions of these molecules such as membrane trafficking, receptor transport, cell signaling, and endocytosis. Using laser scanning confocal microscopy and reflection interference microscopy (RIM), we studied the spatial and temporal distributions of membrane rafts and surface receptors, signaling molecules, and cell organelles during the formation of phagocytic contact areas. K562 cells, which naturally express CD32A, a cell surface receptor for the Fc portion of Immuno-globulin g (IgG), was chosen as a model for neutrophils. An opsonized target was modeled using a glass supported lipid bilayer reconstituted with IgG. CD32A was found to cluster and co-localize with membrane rafts. Placing the K562 cells on the lipid bilayer triggered a process of contact area formation that includes binding between receptors and ligands, their recruitment to the contact area, a concurrent membrane raft movement to and concentration in the contact area, and transport of CD32A, IgG, and membrane rafts to the Golgi complex. Characterization of these processes was performed using agents known to disrupt detergent resistant membranes (DRMs), dissolve actin microfilaments, and inhibit myosin motor activity, which abolished the CD32A clusters and prevented the contact area formation. The relevance to phagocytosis of contact area formation between K562 cells and lipid bilayers was demonstrated using micro-beads coated with a lipid bilayer reconstituted with IgG as the opsonized target instead of the glass supported planar lipid bilayer. Disruption of membrane rafts, salvation of the actin cytoskeleton, and inhibition of myosin II activity were found to inhibit phagocytosis. Here we have provided evidence that membrane rafts serve as platforms that are used to pre-cluster CD32A and transport CD32A along the actin cytoskeleton to the site of phagocytic synapse formation, followed by internalization to the Golgi complex.
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Phan, Toan Anh. "Ocular immunomodulating neuropeptides alpha-MSH and neuropeptide Y modulate phagocytic activity of the microphage cell line RAW 246.7." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12591.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The eye is an immune privileged tissue. Within the ocular microenvironment, there are regulatory mechanisms that suppress inflammation. These anti-inflammatory mechanisms are partly mediated by immunomodulating neuropeptides. We previously found that alpha-melanocyte stimulating hormone (α-MSH) and Neuropeptide Y (NPY) together induce activation of myeloid suppressor-like macrophages. In this study, we examined the possibility that α-MSH and NPY also modulate phagocytosis by macrophages. The monocytic cell line RAW 246.7 was treated with α-MSH and NPY at 1 ng/ml each, a concentration produced by retinal pigment epithelial cells in culture. The treated cells were fed florescent bioparticles of Gram(-) E. Coli or Gram(+) S. Aureus with or without opsin and assayed by flow cytometry. Also tested were the formation of phagolysosomes using pH sensitive florescent E. Coli or S. Aureus bioparticles with or without opsin, and the level of mannose receptors. The a MSH and NPY treated macrophages were significantly suppressed in their capacity to phagocytize unopsonized E. coli; however, suppression of S. Aureus phagocytosis was limited to NPY treated macrophages. In addition, α-MSH and NPY co-treatment suppressed phagocytosis and phagolysosome formation in the macrophages. Fluorescent microscopy imaging showed that there was a qualitative change in phagolysosome formation in opsonized bioparticle conjugates corresponding to the change seen in relative intensity measurements. There was no significant change in the number of man nose receptors in α-MSH, NPY, or α-MSH and NPY treated cells. As α-MSH and NPY together can induce suppressor macrophages within the ocular microenvironment, they can also modulate in a stimulus-dependent manner phagocytic signals within the macrophages. Therefore while the eye is protecting itself from the damaging effects of inflammation it may be making itself vulnerable by having less than optimal innate immune clearance of infectious pathogens.
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Moghimi, S. Moein. "Tissue specific opsonins for phagocytic cells." Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47572.

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Books on the topic "Phagocytic cell"

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Cabello, Felipe C., and Carla Pruzzo, eds. Bacteria, Complement and the Phagocytic Cell. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8.

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1942-, Cabello Felipe C., Pruzzo Carla, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Bacteria, complement, and the phagocytic cell. Berlin: Springer-Verlag, 1988.

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Gabriel, Lopez-Berestein, and Klostergaard Jim, eds. Mononuclear phagocytes in cell biology. Boca Raton, Fla: CRC, 1993.

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R, Ambruso Daniel, ed. Phagocyte production and function following burn injury. Austin: R.G. Landes, 1994.

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van, Furth Ralph, ed. Hemopoietic growth factors and mononuclear phagocytes. Basel: New York, 1993.

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Panea, Casandra M. The role of intestinal mononuclear phagocytes in control of mucosal T cell homeostasis. [New York, N.Y.?]: [publisher not identified], 2016.

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Paul, Robinson J., and Babcock George F. 1948-, eds. Phagocyte function: A guide for research and clinical evaluation. New York: Wiley-Liss, 1998.

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1950-, Grinstein Sergio, and Rotstein Ori D, eds. Mechanisms of leukocyte activation. San Diego: Academic Press, 1990.

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Krysko, Dmitri V. Phagocytosis of dying cells: From molecular mechanisms to human diseases. [Dordrecht]: Springer, 2009.

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J, Sbarra Anthony, and Strauss Robert R, eds. The Respiratory burst and its physiological significance. New York: Plenum Press, 1988.

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Book chapters on the topic "Phagocytic cell"

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Cunningham-Rundles, Charlotte. "Phagocytic Cell Disorders." In Allergy and Clinical Immunology, 408–14. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118609125.ch50.

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De la Fuente, Mónica, and Sonia Medina. "NPY and phagocytic cell functions." In The NPY Family of Peptides in Immune Disorders, Inflammation, Angiogenesis and Cancer, 107–22. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7427-6_6.

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Speert, David P. "Pseudomonas aeruginosa-Phagocytic Cell Interactions." In Pseudomonas aeruginosa as an Opportunistic Pathogen, 163–81. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3036-7_9.

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Gachanja, Naomi N., David A. Dorward, Adriano G. Rossi, and Christopher D. Lucas. "Assays of Eosinophil Apoptosis and Phagocytic Uptake." In Methods in Molecular Biology, 113–32. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1095-4_10.

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AbstractEosinophil apoptosis (programmed cell death) plays an important role in several inflammatory and allergic conditions. Apoptosis triggers various mechanisms including activation of cysteine-aspartic proteases (caspases) and is characterized by morphological and biochemical changes. These include cellular condensation, nuclear fragmentation, increased mitochondrial permeability with loss of membrane potential, and exposure of phosphatidylserine on the cell membrane. A greater understanding of apoptotic mechanisms, subsequent phagocytosis (efferocytosis), and regulation of these processes is critical to understanding disease pathogenesis and development of potential novel therapeutic agents. Release of soluble factors and alterations to surface marker expression by eosinophils undergoing apoptosis aid them in signaling their presence to the immediate environment, and their subsequent recognition by phagocytic cells such as macrophages. Uptake of apoptotic cells usually suppresses inflammation by restricting proinflammatory responses and promoting anti-inflammatory and tissue repair responses. This, in turn, promotes resolution of inflammation. Defects in the apoptotic or efferocytosis mechanisms perpetuate inflammation, resulting in chronic inflammation and enhanced disease severity. This can be due to increased eosinophil life span or cell necrosis characterized by loss of cell membrane integrity and release of toxic intracellular mediators. In this chapter, we detail some of the key assays that are used to assess eosinophil apoptosis, as well as the intracellular signaling pathways involved and phagocytic clearance of these cells.
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García-García, Erick, and Carlos Rosales. "Adding Complexity to Phagocytic Signaling: Phagocytosis-Associated Cell Responses and Phagocytic Efficiency." In Molecular Mechanisms of Phagocytosis, 58–71. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-28669-3_5.

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Schwarz, U. "The Murein Sacculus, the Bacterial Exoskeleton-Structure and Function in the Bacterium and Possible Role in the Host Organism." In Bacteria, Complement and the Phagocytic Cell, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8_1.

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Taylor, Peter W. "The Mode of C5b-9 Attack on Susceptible Gram Negative Bacteria." In Bacteria, Complement and the Phagocytic Cell, 129–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8_10.

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Joiner, K., V. Jiménez-Lucho, N. Grossman, J. Foulds, M. Frank, and L. Leive. "Salmonella and Complement: The Critical Influence of O-Polysaccharide within LPS." In Bacteria, Complement and the Phagocytic Cell, 139–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8_11.

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Mäkelä, P. Helena, Marianne Hovi, Harri Saxen, Matti Valtonen, and Ville Valtonen. "Ability to Activate the Alternative Complement Pathway as a Virulence Determinant in Salmonellae." In Bacteria, Complement and the Phagocytic Cell, 157–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8_12.

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Moxon, E. R., and J. A. Winkelstein. "Interaction of Haemophilus Influenzae with Complement." In Bacteria, Complement and the Phagocytic Cell, 177–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8_13.

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Conference papers on the topic "Phagocytic cell"

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Minamitani, H., T. Shimomura, M. Aiba, and E. Okada. "Magnetophoresis for mononuclear cell separation and diagnostic evaluation of the phagocytic capacity of monocyte." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1988. http://dx.doi.org/10.1109/iembs.1988.95127.

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Ween, M., N. Bastian, and L. Thredgold. "E-cigarette Coil Metal Composition Contributes to Epithelial Cell Toxicity and Macrophage Phagocytic Dysfunction." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1226.

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Shah, Neha B., and John C. Bischof. "Effect of Surface Charge on Gold Nanoparticle Biotransport: An In Vivo Blood and Biodistribution Study." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53324.

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Intravenously injected nanoparticles (NPs) hold great promise for clinical diagnostic and therapeutic applications. While several NPs for such clinical applications have emerged in various designs (metallic, polymeric, quantum dots etc.) [1], a critical issue in their in vivo use is the lack of fundamental studies examining the effects of physicochemical parameters (shape, size, surface properties etc.) on blood circulation, kinetics of accumulation and elimination as well as toxicity [2–4]. We hypothesize that blood, the first medium of interaction in the body, is a major determinant of biotransport and biodistribution. Recent and past in vitro studies have shown that NPs interact with serum proteins (including complement factors), cause platelet aggregation and red blood cell hemolysis, and are taken up by phagocytic cells. However, to our knowledge a detailed in vivo study of the interaction of metallic nanoparticles with blood components as a function of their surface properties does not yet exist.
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Shands, J. W., T. D. Sunnenberg, and R. Lottenberg. "TISSUE FACTOR AND FACTOR VII PRODUCTION BY MURINE BONE MARROW-DERIVED MACROPHAGES:." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643288.

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Monocytes and macrophages (macs) make factor VII (VII) and can be induced to make tissue factor (TF), but when during differentiation this capacity is acquired is unknown. We approached this by measuring the synthesis of these factors by bone marrow cells (BMC) during in vitro differentiation into mature macs. BMC were harvested and cultured in RPMI-1640 supplemented with 15mM HEPES buffer, gentamicin, 10% FCS, 15% L-cell conditioned medium, and 2 mM L-glutamine. At intervals, characteristics of macs were measured: size, staining for non-specific esterase, phagocytosis of IgG sensitized RBC, induction of TF by a 6 hr exposure to endotoxin (LPS), and production of VII. The cells increased in mean diameter from 8.5u on d 1 to 15u on d 7 and to 17u on d 15. On d 2-3 of culture few cells were esterase pos, but 51% were phagocytic. By d 7, 95% were esterase pos and phagocytic. After 5 d of culture, macs spontaneously produced small amts of TF as measured by a coupled amidolytic assay. This increased 3 X over the total 15 d of culture. Two d macs did not synthesize TF in response to 1 ug/ml LPS. Responsiveness to LPS began at d 5 and reached a maximum between d 7 and 10 (5X control). The lack of response of 2-3 d macs was not due to suppressor cells, since mixing these with 10 d cells failed to blunt the response of the latter. VII, also measured by a coupled amidolytic assay, was produced on d 2, maximally on d 5, and decreased thereafter. It was not influenced by a 6 hr "induction" with LPS. BMC cultured in the continuous presence of 50 ng/ml LPS were incapable of producing VII and TF. These data suggest that immature macs can synthesize factor VII but not TF and that TF and factor VII synthesis are not coordinately expressed during mac maturation. Culture of BMC in the continuous presence of 50 ng/ml of LPS shut down the production of the coagulant factors by unknown means.
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Aires, Patricia Pontes. "In vitro model for monogenic Behçet’s disease: analysis of phagocytosis, oxidative metabolism and proliferation in phagocytic mutated cell lineages." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.2139.

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Vieira, Jussane Oliveira, Hugo Leite de Farias Brito, and Jeronimo Gonçalves de Araújo. "GRANULOMATOUS MASTITIS CAUSED BY HISTOPLASMA CAPSULATUM." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1039.

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Histoplasma is a thermally dimorphic fungus with endemic and opportunistic behavior, which causes a systemic disease known as histoplasmosis. The habitat for this fungus is soil laden with bird and bat droppings, in caves and henhouses, and it persists in the environment long after the contamination. This fungus is widely disseminated in the American continent. In South American countries, the disease is mainly present in Venezuela, Colombia, Peru, Brazil, Argentina, and Uruguay. Man is contaminated by inhaling conidia present in nature, and most infections are mild and subclinical. After being inhaled, conidia undergo phagocytosis by macrophages and mononuclear cells, which are unable to destroy them. They multiply inside these cells, traveling through mediastinal and hilar lymph nodes and into the bloodstream, spleen, bone marrow, liver, skin, and subcutaneous tissue. The diagnosis is based on the detection of the fungus in secretions or tissues and in serology tests. Among these tests, enzyme-linked immunosorbent assays are more sensitive and specific than complement fixation. Tissue biopsies show epithelioid granulomas, with or without necrosis, and fungi within phagocytic cells. Gomori-Groccot staining is required for the visualization of the fungus. A 22-year-old female patient, an undergraduate psychology student, from the urban area of the inner state of Sergipe, no comorbidities, vegetarian, visited a mastologist due to the recent appearance of a nodule in the right breast associated with signs of inflammation and no fever. The clinical examination showed a 2 cm palpable, retroareolar thickening, and thickening of the areolar skin with discrete hyperemia, and no palpable axillary lymph nodes. The patient was initially treated with amoxicillin and clavulanic acid for 7 days. After treatment, there was regression of the inflammation signs upon physical examination; however, the thickening remained and the areolar skin was still thickened and hard. An ultrasound of the right breast showed a well-defined heterogeneous, superficial, and elongated retroareolar nodular image, measuring 3.4×1.2 cm. A breast ultrasound-guided fine-needle aspiration (FNA) was performed, and the cytology test suggested an inflammatory process. After 1 month, the patient returned with two areolar fistulas with yellowish discharge. A new cycle of antimicrobial therapy was started with clindamycin for 14 days. The secretion was decreased over the antibiotic period; however, 14 days after the treatment, the two areolar fistulas were still present with yellowish discharge. A third cycle of antibiotic therapy with metronidazole was administered with no improvement. An excisional biopsy was performed of the area around the fistula and the underlying breast tissue. Two specimens were examined — one skin specimen with the fistulizing areas measuring 1.9×0.8×0.8 cm, and the other specimen measuring 1.7 cm, corresponding to the breast tissue beyond the fistulas, measuring 1.7×1×0.2 cm. Histopathological evaluation of the specimen showed a chronic, granulomatous inflammatory process, with exudative foci and formation of a fistulous tract, chronic inflammatory lymphoplasmacytic reaction, fibrosis, and giant cell reaction. Screening for fungi (Groccot) showed small, clustered yeast-like structures in the cytoplasm of macrophages, suggestive of histoplasmosis. The patient’s clinical tests included hemoglobin of 9 and a white blood cell count of 3,500, with a normal differential count. Screenings for HIV, hepatitis B, and hepatitis C were negative, fasting blood glucose was normal, and liver function was normal. The anemia investigation revealed only a ferroprivic component because of the vegetarian diet. The patient was subjected to general chest and abdominal examinations with no abnormalities. The patient was started on itraconazole 200 mg a day for 1 year, with no relapse until the end of the treatment.
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Awasthi, S., R. Wolf, and G. White. "Immunophenotype and Phagocytic Function of Preterm Fetal Baboon Lung Dendritic Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3281.

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Latina, M. A., P. H. Kobsa, S. L. Rakestraw, E. A. Crean, T. Hasan, and M. L. Yarmush. "Photochemical Targeting Of Phagocytic Trabecular Meshwork Cells Using Chlorin E6 Coupled Microspheres." In O-E/Fiber LASE '88, edited by Tayyaba Hasan. SPIE, 1989. http://dx.doi.org/10.1117/12.960182.

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Dewidar, B., S. Hammad, HL Weng, MP Ebert, JG Hengstler, and S. Dooley. "Jagged-1 expression in stressed hepatocytes enhances phagocytic activity of Kupffer cells." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605073.

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Nachman, R. L., R. L. Silverstein, and A. S. Asch. "THROMBOSPONDIN: CELL BIOLOGY OF AN ADHESIVE GLYCOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644653.

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Thrombospondin (TSP), a multifunctional 450 KD glycoprotein is a secretory product of thrombin stimulated platelets. It is a major component of the platelets alpha granule constituting approximately 3% of total platelet protein. Thrombospondin does not circulate in appreciable concentrations ∽0 100 ng/ml); however, the tissue distribution is broad. In addition to its expression on the membrane of activated platelets, the protein is synthesized by fibroblasts endothelial cells, glial cell smooth muscle cells alveolar pneumocytes mononuclear phagocytes and various tumor cells. TSP is a major constituent of the extracellular matrix and has been demonstrated in the vessel wall, basement membrane and glandular connective tissue. Fibroblasts, smooth muscle cells and endothelial cells in tissue culture incorporate TSP into the extracellular matrix. Matrix TSP is under cell-cycle regulatory control. Mesenchymal cells in the proliferative phase synthesize greater amounts of TSP than non growing cells. Platelet derived growth factor induces smooth muscle cell and glial cell synthesis of TSP. Atheromatous lesions contain increased amounts of TSP compared to normal vessels emphasizing the potential role of TSP in the interaction of proliferating cells with the matrix. TSP binds specifically, saturably, and reversibly to mouse peritoneal macrophages and to cells of the monocyte-like human cell line U937. Binding was time dependent and was optimal in the presence of both Ca++ and Mg++. PMA stimulated U937 cells and activated macrophages bound TSP to an equivalent extent as resting cells. The TSP binding site on the surface of U937 cells and peripheral blood monocytes mediates the adhesive interaction between these cells and thrombin-stimulated platelets. Using a sensitive rosetting assay we found that monocytes were not rosetted by resting platelets while >90% were rosetted by thrombin-stimulated platelets. Monoclonal and polyclonal anti-TSP antibodies markedly inhibited rosetting as did TSP itself. Antifibronectin or non-immune control antibodies did not inhibit rosetting, nor did fibronectin, fibrinogen, the fibronectinadhesion tetrapeptide arg-gly-asp-ser (RGDS), or heparin. The TSP membrane receptor, an 88 KD glycoprotein, formely known as GPIV has been identified in platelets, endothelial cells, monocytes and a variety of tumor cells. TSP may thus serve as a molecular bridge linking activated platelets with monocytes at sites of early vascular injury. Such interactions involving the TSP receptor complex may be of critical importance in the regulation of thrombosis and the initiation of atherosclerosis.
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Reports on the topic "Phagocytic cell"

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Elliott, Michael R. Enhancing the Phagocytic Clearance of Apoptotic Cells to Control Breast Carcinoma Progression. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566560.

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Elliott, Michael R. Enhancing the Phagocytic Clearance of Apoptotic Cells to Control Breast Carcinoma Progression. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada548991.

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Bercovier, Herve, Raul Barletta, and Shlomo Sela. Characterization and Immunogenicity of Mycobacterium paratuberculosis Secreted and Cellular Proteins. United States Department of Agriculture, January 1996. http://dx.doi.org/10.32747/1996.7573078.bard.

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Our long-term goal is to develop an efficient acellular vaccine against paratuberculosis based on protein antigen(s). A prerequisite to achieve this goal is to analyze and characterize Mycobacterium paratuberculosis (Mpt) secreted and cellular proteins eliciting a protective immune response. In the context of this general objective, we proposed to identify, clone, produce, and characterize: the Mpt 85B antigen and other Mpt immunoreactive secreted proteins, the Mpt L7/L12 ribosomal protein and other immunoreactive cellular proteins, Mpt protein determinants involved in invasion of epithelial cells, and Mpt protein antigens specifically expressed in macrophages. Paratuberculosis is still a very serious problem in Israel and in the USA. In the USA, a recent survey evaluated that 21.6% of the dairy herd were infected with Mpt resulting in 200-250 million dollars in annual losses. Very little is known on the virulence factors and on protective antigens of Mpt. At present, the only means of controlling this disease are culling or vaccination. The current vaccines do not allow a clear differentiation between infected and vaccinated animals. Our long-term goal is to develop an efficient acellular paratuberculosis vaccine based on Mpt protein antigen(s) compatible with diagnostic tests. To achieve this goal it is necessary to analyze and characterize secreted and cellular proteins candidate for such a vaccine. Representative Mpt libraries (shuttle plasmid and phage) were constructed and used to study Mpt genes and gene products described below and will be made available to other research groups. In addition, two approaches were performed which did not yield the expected results. Mav or Mpt DNA genes that confer upon Msg or E. coli the ability to invade and/or survive within HEp-2 cells were not identified. Likewise, we were unable to characterize the 34-39 kDa induced secreted proteins induced by stress factors due to technical difficulties inherent to the complexity of the media needed to support substantial M. pt growth. We identified, isolated, sequenced five Mpt proteins and expressed four of them as recombinant proteins that allowed the study of their immunological properties in sensitized mice. The AphC protein, found to be up regulated by low iron environment, and the SOD protein are both involved in protecting mycobacteria against damage and killing by reactive oxygen (Sod) and nitrogen (AhpC) intermediates, the main bactericidal mechanisms of phagocytic cells. SOD and L7/L12 ribosomal proteins are structural proteins constitutively expressed. 85B and CFP20 are both secreted proteins. SOD, L7/L12, 85B and CFP20 were shown to induce a Th1 response in immunized mice whereas AphC was shown by others to have a similar activity. These proteins did not interfere with the DTH reaction of naturally infected cows. Cellular immunity provides protection in mycobacterial infections, therefore molecules inducing cellular immunity and preferentially a Th1 pathway will be the best candidate for the development of an acellular vaccine. The proteins characterized in this grant that induce a cell-mediated immunity and seem compatible with diagnostic tests, are good candidates for the construction of a future acellular vaccine.
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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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