Статті в журналах: "Phagocytic cell"

1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Guo, Feiye, Ying Ding, Nora Caberoy, Gabriela Alvarado, Feng Wang, Rui Chen, and Wei Li. "ABCF1 extrinsically regulates retinal pigment epithelial cell phagocytosis." Molecular Biology of the Cell 26, no. 12 (June 15, 2015): 2311–20. http://dx.doi.org/10.1091/mbc.e14-09-1343.

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Phagocytosis of shed photoreceptor outer segments (POSs) by retinal pigment epithelial (RPE) cells is critical to retinal homeostasis and shares many conserved signaling pathways with other phagocytes, including extrinsic regulations. Phagocytotic ligands are the key to cargo recognition, engulfment initiation, and activity regulation. In this study, we identified intracellular protein ATP-binding cassette subfamily F member 1 (ABCF1) as a novel RPE phagocytotic ligand by a new approach of functional screening. ABCF1 was independently verified to extrinsically promote phagocytosis of shed POSs by D407 RPE cells. This finding was further corroborated with primary RPE cells and RPE explants. Internalized POS vesicles were colocalized with a phagosome marker, suggesting that ABCF1-mediated engulfment is through a phagocytic pathway. ABCF1 was released from apoptotic cells and selectively bound to shed POS vesicles and apoptotic cells, possibly via externalized phosphatidylserine. ABCF1 is predominantly expressed in POSs and colocalized with the POS marker rhodopsin, providing geographical convenience for regulation of RPE phagocytosis. Collectively these results suggest that ABCF1 is released from and binds to shed POSs in an autocrine manner to facilitate RPE phagocytosis through a conserved pathway. Furthermore, the new approach is broadly applicable to many other phagocytes and will enable systematic elucidation of their ligands to understand extrinsic regulation and cargo recognition.

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12

Ren, Y., R. L. Silverstein, J. Allen, and J. Savill. "CD36 gene transfer confers capacity for phagocytosis of cells undergoing apoptosis." Journal of Experimental Medicine 181, no. 5 (May 1, 1995): 1857–62. http://dx.doi.org/10.1084/jem.181.5.1857.

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Phagocyte recognition and ingestion of intact cells undergoing apoptosis are key events in this generally important program of cell death. Insufficient phagocyte capacity for apoptotic cells can result in failure to clear dying cells before membrane integrity is lost, resulting in leakage of noxious cell contents and severe tissue damage. However, no means has been available to increase phagocytic clearance of apoptotic cells. We now report that transfection of the macrophage adhesion molecule CD36 into human Bowes melanoma cells specifically conferred greatly increased capacity to ingest apoptotic neutrophils, lymphocytes, and fibroblasts, comparable to that exhibited by macrophages. Furthermore, when CD36 was transfected into another cell type with limited capacity to take up apoptotic bodies, the monkey COS-7 cell, similar effects were observed. Therefore, CD36 gene transfer can confer "professional" capacity to ingest apoptotic cells upon "amateur" phagocytes.

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13

Patil, Mallikarjun, Sherin Saheera, Praveen K. Dubey, Asher Kahn-Krell, Prem Kumar Govindappa, Sarojini Singh, Sultan Tousif, et al. "Novel Mechanisms of Exosome-Mediated Phagocytosis of Dead Cells in Injured Heart." Circulation Research 129, no. 11 (November 12, 2021): 1006–20. http://dx.doi.org/10.1161/circresaha.120.317900.

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Rationale: After myocardial ischemic injury, improper phagocytic clearance of dying cardiac cells and the ensuing lack of inflammation resolution results in adverse cardiac remodeling and dysfunction that might lead to heart failure. Therefore, therapeutic strategies to ameliorate immune cell phagocytic function are critical for augmenting cardiac repair after injury. Objective: To determine whether mesenchymal stem cell–derived exosomes (MSC-Exos) act as opsonin for apoptotic cells or trigger eat-me phagocytic signaling in resident/recruited phagocytes after myocardial ischemic injury. Methods and Results: We evaluated MSC-Exo–mediated opsonization of apoptotic cardiomyocytes and in vitro and in vivo effects of MFGE8 (milk fat globule epidermal growth factor-factor VIII)-deficient mouse MSC-Exo on macrophage engulfment of apoptotic cardiomyocytes and its implications on cardiac remodeling, repair, and function. Microscopy and FACS analyses show that opsonization of apoptotic cardiomyocytes with MSC-Exo enhances their engulfment by macrophages. Furthermore, preincubation of macrophages with MSC-Exo reprogrammed the signaling pathways involved in phagocytosis and expression of proreparative cytokines. Protein analysis of MSC-Exo reveals expression of MFGE8—a glycoprotein that bridges externalized phosphatidylserine on the apoptotic cell surface to αVβ3 or αVβ5 integrins on the phagocyte. Most intriguingly, siRNA inhibition of MFGE8 significantly reduced the MSC-Exo–mediated augmentation of dead cell engulfment, associated signaling, and proreparative phenotype. After myocardial ischemic injury, intramyocardial administration of MSC-Exo increases macrophage uptake of apoptotic bodies in the border zone of infarct and is associated with reduced proinflammatory response, increase in neovascularization, lower infarct size, and an improvement in cardiac function and MFGE8-deficient MSC-Exo administration failed to protect mice against myocardial infarction. Conclusions: Our data demonstrate that exosome-associated MFGE8 on one hand enhances opsonization of dead cells and on the other activates phagocytic signaling, thus augmenting removal of apoptotic cells, resolution of inflammation, and, therefore, efficient cardiac recovery after injury.

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14

Brill-Karniely, Yifat, Dvir Dror, Tal Duanis-Assaf, Yoel Goldstein, Ouri Schwob, Talya Millo, Natalie Orehov, et al. "Triangular correlation (TrC) between cancer aggressiveness, cell uptake capability, and cell deformability." Science Advances 6, no. 3 (January 2020): eaax2861. http://dx.doi.org/10.1126/sciadv.aax2861.

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The malignancy potential is correlated with the mechanical deformability of the cancer cells. However, mechanical tests for clinical applications are limited. We present here a Triangular Correlation (TrC) between cell deformability, phagocytic capacity, and cancer aggressiveness, suggesting that phagocytic measurements can be a mechanical surrogate marker of malignancy. The TrC was proved in human prostate cancer cells with different malignancy potential, and in human bladder cancer and melanoma cells that were sorted into subpopulations based solely on their phagocytic capacity. The more phagocytic subpopulations showed elevated aggressiveness ex vivo and in vivo. The uptake potential was preserved, and differences in gene expression and in epigenetic signature were detected. In all cases, enhanced phagocytic and aggressiveness phenotypes were correlated with greater cell deformability and predicted by a computational model. Our multidisciplinary study provides the proof of concept that phagocytic measurements can be applied for cancer diagnostics and precision medicine.

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15

Fibbe, WE, J. van Damme, A. Billiau, PJ Voogt, N. Duinkerken, PM Kluck, and JH Falkenburg. "Interleukin-1 (22-K factor) induces release of granulocyte-macrophage colony-stimulating activity from human mononuclear phagocytes." Blood 68, no. 6 (December 1, 1986): 1316–21. http://dx.doi.org/10.1182/blood.v68.6.1316.1316.

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Abstract An electrophoretically pure preparation of natural human interleukin-1 (IL-1) was shown to stimulate in vitro colony formation in human bone marrow cultures. Day 4 myeloid cluster-forming cells (CFC), as well as early (day 7) and late (day 10) granulocyte-macrophage colony-forming units (CFU-GM) were stimulated in a dose-dependent fashion. At optimal concentrations of IL-1, the number of day 4 CFC reached 72%, the number of day 7 CFU-GM reached 32%, and the number of day 10 CFU-GM reached 80% of the respective numbers of colonies obtained by addition of crude leukocyte-conditioned medium (LCM). The IL-1-induced stimulatory effect on CFU-GM growth could be completely neutralized by a rabbit anti-IL-1 antiserum. Colony growth was abrogated by depleting the marrow cell suspensions of phagocytic cells prior to IL-1 addition. Conversely, the effect could be reintroduced by addition of marrow-derived adherent cells to bone marrow cell suspensions that had been depleted of both phagocytic and E rosetting T cells. Furthermore, media conditioned by bone marrow-derived adherent cells or by peripheral blood mononuclear phagocytes in the presence but not in the absence of IL-1, stimulated in vitro colony growth of phagocyte-depleted bone marrow cell suspensions. These results indicate that IL-1 induces release of granulocyte-macrophage colony-stimulating activity (GM-CSA) from human mononuclear phagocytes.

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16

Fibbe, WE, J. van Damme, A. Billiau, PJ Voogt, N. Duinkerken, PM Kluck, and JH Falkenburg. "Interleukin-1 (22-K factor) induces release of granulocyte-macrophage colony-stimulating activity from human mononuclear phagocytes." Blood 68, no. 6 (December 1, 1986): 1316–21. http://dx.doi.org/10.1182/blood.v68.6.1316.bloodjournal6861316.

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An electrophoretically pure preparation of natural human interleukin-1 (IL-1) was shown to stimulate in vitro colony formation in human bone marrow cultures. Day 4 myeloid cluster-forming cells (CFC), as well as early (day 7) and late (day 10) granulocyte-macrophage colony-forming units (CFU-GM) were stimulated in a dose-dependent fashion. At optimal concentrations of IL-1, the number of day 4 CFC reached 72%, the number of day 7 CFU-GM reached 32%, and the number of day 10 CFU-GM reached 80% of the respective numbers of colonies obtained by addition of crude leukocyte-conditioned medium (LCM). The IL-1-induced stimulatory effect on CFU-GM growth could be completely neutralized by a rabbit anti-IL-1 antiserum. Colony growth was abrogated by depleting the marrow cell suspensions of phagocytic cells prior to IL-1 addition. Conversely, the effect could be reintroduced by addition of marrow-derived adherent cells to bone marrow cell suspensions that had been depleted of both phagocytic and E rosetting T cells. Furthermore, media conditioned by bone marrow-derived adherent cells or by peripheral blood mononuclear phagocytes in the presence but not in the absence of IL-1, stimulated in vitro colony growth of phagocyte-depleted bone marrow cell suspensions. These results indicate that IL-1 induces release of granulocyte-macrophage colony-stimulating activity (GM-CSA) from human mononuclear phagocytes.

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17

du Preez, Kelly, Yolandi Rautenbach, Emma H. Hooijberg, and Amelia Goddard. "Oxidative burst and phagocytic activity of phagocytes in canine parvoviral enteritis." Journal of Veterinary Diagnostic Investigation 33, no. 5 (June 19, 2021): 884–93. http://dx.doi.org/10.1177/10406387211025513.

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Canine parvoviral enteritis (CPE) is a severe disease characterized by systemic inflammation and immunosuppression. The function of circulating phagocytes (neutrophils and monocytes) in affected dogs has not been fully investigated. We characterized the functional capacity of canine phagocytes in CPE by determining their oxidative burst and phagocytic activities using flow cytometry. Blood was collected from 28 dogs with CPE and 11 healthy, age-matched, control dogs. Oxidative burst activity was assessed by stimulating phagocytes with opsonized Escherichia coli or phorbol 12-myristate 13-acetate (PMA) and measuring the percentage of phagocytes producing reactive oxygen species and the magnitude of this production. Phagocytosis was measured by incubating phagocytes with opsonized E. coli and measuring the percentage of phagocytes containing E. coli and the number of bacteria per cell. Complete blood counts and serum C-reactive protein (CRP) concentrations were also determined. Serum CRP concentration was negatively and positively correlated with segmented and band neutrophil concentrations, respectively. Overall, no differences in phagocyte function were found between dogs with CPE and healthy control dogs. However, infected dogs with neutropenia or circulating band neutrophils had decreased PMA-stimulated oxidative burst activity compared to healthy controls. Additionally, CPE dogs with neutropenia or circulating band neutrophils had decreased PMA- and E. coli–stimulated oxidative burst activity and decreased phagocytosis of E. coli compared to CPE dogs without neutropenia or band neutrophils. We conclude that phagocytes have decreased oxidative burst and phagocytic activity in neutropenic CPE dogs and in CPE dogs with circulating band neutrophils.

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18

Alva-Murillo, Nayeli, Joel Edmundo López-Meza, and Alejandra Ochoa-Zarzosa. "Nonprofessional Phagocytic Cell Receptors Involved inStaphylococcus aureusInternalization." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/538546.

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Staphylococcus aureusis a successful human and animal pathogen. The majority of infections caused by this pathogen are life threatening, primarily becauseS. aureushas developed multiple evasion strategies, possesses intracellular persistence for long periods, and targets the skin and soft tissues. Therefore, it is very important to understand the mechanisms employed byS. aureusto colonize and proliferate in these cells. The aim of this review is to describe the recent discoveries concerning the host receptors of nonprofessional phagocytes involved inS. aureusinternalization. Most of the knowledge related to the interaction ofS. aureuswith its host cells has been described in professional phagocytic cells such as macrophages. Here, we showed that in nonprofessional phagocytes theα5β1 integrin host receptor, chaperons, and the scavenger receptor CD36 are the main receptors employed duringS. aureusinternalization. The characterization and identification of new bacterial effectors and the host cell receptors involved will undoubtedly lead to new discoveries with beneficial purposes.

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Winstel, Volker, Dominique Missiakas, and Olaf Schneewind. "Staphylococcus aureustargets the purine salvage pathway to kill phagocytes." Proceedings of the National Academy of Sciences 115, no. 26 (June 11, 2018): 6846–51. http://dx.doi.org/10.1073/pnas.1805622115.

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Staphylococcus aureuscolonizes large segments of the human population and causes invasive infections due to its ability to escape phagocytic clearance. During infection, staphylococcal nuclease and adenosine synthase A convert neutrophil extracellular traps to deoxyadenosine (dAdo), which kills phagocytes. The mechanism whereby staphylococcal dAdo intoxicates phagocytes is not known. Here we used CRISPR-Cas9 mutagenesis to show that phagocyte intoxication involves uptake of dAdo via the human equilibrative nucleoside transporter 1, dAdo conversion to dAMP by deoxycytidine kinase and adenosine kinase, and signaling via subsequent dATP formation to activate caspase-3–induced cell death. Disruption of this signaling cascade confers resistance to dAdo-induced intoxication of phagocytes and may provide therapeutic opportunities for the treatment of infections caused by antibiotic-resistantS. aureusstrains.

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20

O'Keeffe, Kate M., Mieszko M. Wilk, John M. Leech, Alison G. Murphy, Maisem Laabei, Ian R. Monk, Ruth C. Massey, et al. "Manipulation of Autophagy in Phagocytes Facilitates Staphylococcus aureus Bloodstream Infection." Infection and Immunity 83, no. 9 (June 22, 2015): 3445–57. http://dx.doi.org/10.1128/iai.00358-15.

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The capacity for intracellular survival within phagocytes is likely a critical factor facilitating the dissemination ofStaphylococcus aureusin the host. To date, the majority of work onS. aureus-phagocyte interactions has focused on neutrophils and, to a lesser extent, macrophages, yet we understand little about the role played by dendritic cells (DCs) in the direct killing of this bacterium. Using bone marrow-derived DCs (BMDCs), we demonstrate for the first time that DCs can effectively killS. aureusbut that certain strains ofS. aureushave the capacity to evade DC (and macrophage) killing by manipulation of autophagic pathways. Strains with high levels of Agr activity were capable of causing autophagosome accumulation, were not killed by BMDCs, and subsequently escaped from the phagocyte, exerting significant cytotoxic effects. Conversely, strains that exhibited low levels of Agr activity failed to accumulate autophagosomes and were killed by BMDCs. Inhibition of the autophagic pathway by treatment with 3-methyladenine restored the bactericidal effects of BMDCs. Using anin vivomodel of systemic infection, we demonstrated that the ability ofS. aureusstrains to evade phagocytic cell killing and to survive temporarily within phagocytes correlated with persistence in the periphery and that this effect is critically Agr dependent. Taken together, our data suggest that strains ofS. aureusexhibiting high levels of Agr activity are capable of blocking autophagic flux, leading to the accumulation of autophagosomes. Within these autophagosomes, the bacteria are protected from phagocytic killing, thus providing an intracellular survival niche within professional phagocytes, which ultimately facilitates dissemination.

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21

Selsted, Michael E., and Andre J. Ouellette. "Defensins in granules of phagocytic and non-phagocytic cells." Trends in Cell Biology 5, no. 3 (March 1995): 114–19. http://dx.doi.org/10.1016/s0962-8924(00)88961-8.

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22

Wang, Huizhen, Haikun Wang, Weipeng Xiong, Yongmei Chen, Quanhong Ma, Jing Ma, Yehua Ge, and Daishu Han. "Evaluation on the phagocytosis of apoptotic spermatogenic cells by Sertoli cells in vitro through detecting lipid droplet formation by Oil Red O staining." Reproduction 132, no. 3 (September 2006): 485–92. http://dx.doi.org/10.1530/rep.1.01213.

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During spermatogenesis, more than half of the differentiating spermatogenic cells undergo apoptosis before they mature into spermatozoa. Ultrastructure studies showed that the formation of lipid droplets in Sertoli cells was associated with phagocytosis of residual bodies and apoptotic germ cells by Sertoli cells. Here, a relationship between the phagocytosis of apoptotic spermatogenic cells and lipid droplet formation in Sertoli cells was studiedin vitroby Oil Red O (ORO) staining. The results confirmed that the formation of lipid droplets was a result of phagocytosis of apoptotic spermatogenic cells in Sertoli cells. By comparing phagocytosis of apoptotic spermatogenic cells and thymocytes by Sertoli cells to that by macrophages, we demonstrated that the lipid droplets accumulation in phagocytes depended on phagocytosed apoptotic cell type, but not phagocyte type. However, the size of lipid droplets was related to the type of phagocytes. By this approach, we found that Sertoli cells at different postnatal stages of development had a similar phagocytic ability. These results suggested that the detection of lipid droplets by ORO staining was a practical method to evaluate the phagocytic functions of Sertoli cellsin vitro. This approach could also be considered as anin vitromodel to study the lipid formation, metabolism, and function in Sertoli cells.

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Robertson, Maura D., Anthony Seaton, and J. A. Raeburn. "Phagocytic cell responses toAspergillus fumigatus." FEMS Microbiology Letters 47, no. 5 (April 1989): 305–6. http://dx.doi.org/10.1111/j.1574-6968.1989.tb02401.x.

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24

Henricks, P. A. J., J. Verhoef, and F. P. Nijkamp. "Modulation of phagocytic cell function." Veterinary Research Communications 10, no. 1 (December 1986): 165–88. http://dx.doi.org/10.1007/bf02213979.

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Vomund, Anthony N., Bernd H. Zinselmeyer, Jing Hughes, Boris Calderon, Carolina Valderrama, Stephen T. Ferris, Xiaoxiao Wan, et al. "Beta cells transfer vesicles containing insulin to phagocytes for presentation to T cells." Proceedings of the National Academy of Sciences 112, no. 40 (August 31, 2015): E5496—E5502. http://dx.doi.org/10.1073/pnas.1515954112.

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Beta cells from nondiabetic mice transfer secretory vesicles to phagocytic cells. The passage was shown in culture studies where the transfer was probed with CD4 T cells reactive to insulin peptides. Two sets of vesicles were transferred, one containing insulin and another containing catabolites of insulin. The passage required live beta cells in a close cell contact interaction with the phagocytes. It was increased by high glucose concentration and required mobilization of intracellular Ca2+. Live images of beta cell–phagocyte interactions documented the intimacy of the membrane contact and the passage of the granules. The passage was found in beta cells isolated from islets of young nonobese diabetic (NOD) mice and nondiabetic mice as well as from nondiabetic humans. Ultrastructural analysis showed intraislet phagocytes containing vesicles having the distinct morphology of dense-core granules. These findings document a process whereby the contents of secretory granules become available to the immune system.

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Couzinet, Sabine, Elisabeth Cejas, Johannes Schittny, Peter Deplazes, Rainer Weber, and Stefan Zimmerli. "Phagocytic Uptake of Encephalitozoon cuniculi by Nonprofessional Phagocytes." Infection and Immunity 68, no. 12 (December 1, 2000): 6939–45. http://dx.doi.org/10.1128/iai.68.12.6939-6945.2000.

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ABSTRACT Encephalitozoon cuniculi is an obligate intracellular, spore-forming parasite belonging to the microsporidia that can cause disseminated infection in immunocompromised persons. E. cuniculi spores infect host cells by germination, i.e., by explosively everting the polar filament, through which the spore contents (sporoplasms) are subsequently injected into the cytoplasm. In addition, we observed intracellular, nongerminated spores in various nonprofessional phagocytes. In MRC5 cells, the number of internalized spores was approximately 10-fold higher than the number of injected sporoplasms. Compared to the rate of uptake by human monocyte-derived macrophages, internalization rates by A549 cells, MRC5 cells, and 293 cells were 0.6, 4.4, and 22.2%, respectively. The mechanism of uptake was studied in MRC5 cells. Killed spores were internalized at the same rate as live spores, indicating that nongerminated parasites do not actively participate in cell entry. Cytochalasin D inhibited uptake of spores by 95%, demonstrating an actin-dependent process. By electron and epifluorescence microscopy, intracellular spores were found in a tightly fitting membrane-bound compartment. The vacuole containing the spores was positive for the lysosomal membrane protein LAMP-1 and colocalized with the late endosomal-lysosomal content marker rhodamine dextran. Our results show that, in addition to the unique way in which microsporidia infect cells, E. cuniculi spores enter nonprofessional phagocytes by phagocytosis and traffic into a late endosomal-lysosomal compartment.

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Kono, Rena, Yuji Ikegaya, and Ryuta Koyama. "Phagocytic Glial Cells in Brain Homeostasis." Cells 10, no. 6 (May 29, 2021): 1348. http://dx.doi.org/10.3390/cells10061348.

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Phagocytosis by glial cells has been shown to play an important role in maintaining brain homeostasis. Microglia are currently considered to be the major phagocytes in the brain parenchyma, and these cells phagocytose a variety of materials, including dead cell debris, abnormally aggregated proteins, and, interestingly, the functional synapses of living neurons. The intracellular signaling mechanisms that regulate microglial phagocytosis have been studied extensively, and several important factors, including molecules known as “find me” signals and “eat me” signals and receptors on microglia that are involved in phagocytosis, have been identified. In addition, recent studies have revealed that astrocytes, which are another major glial cell in the brain parenchyma, also have phagocytic abilities. In this review, we will discuss the roles of microglia and astrocytes in phagocytosis-mediated brain homeostasis, focusing on the characteristics and differences of their phagocytic abilities.

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Oliynyk, Zh. "LONG-TERM EFFECTS OF SHAM SURGERY ON PHAGOCYTE FUNCTIONS IN RATS." Biotechnologia Acta 15, no. 2 (April 2022): 37–46. http://dx.doi.org/10.15407/biotech15.02.037.

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Animal models of inflammatory disorders, including those of the nervous system are commonly used to explore the pathophysiological role of immune cell response in disease triggering and course and to develop biotechnology products for therapeutic use. Modeling some of these disorders, particularly neurodegenerative diseases, implies surgical manipulations for the intracerebral introduction of disease-initiating substances (toxins, amyloids etc.). Design of these experiments involves the use of sham-operated animals as a control of non-specific intrinsic side-effects elicited by surgical manipulations per se, including local and systemic inflammation, where phagocytic cells are key participants. Short-term post-surgical immunomodulatory effects are widely reported. However, no study thus far has examined the long term effects of sham-surgery on phagocyte functions. The purpose of this study was to evaluate the effect of sham-surgery, commonly used for modeling neurodegenerative diseases, on phagocyte functions in the far terms after the surgical manipulations. Materials and Methods. Adult male Wistar rats were used in the study. Sham surgery consisted of stereotactic unilateral injection of saline solution into the median forebrain bundle (sham-operated 1, SO1) or directly into the substantia nigra (sham-operated 2, SO2). Before the placebo surgery, animals were anaesthetized using nembutal and ketamine/xylazine correspondingly. Functional characteristics (phagocytic activity, oxidative metabolism, CD80/86 and CD206 expression) of phagocytes (microglia, peritoneal macrophages, circulating monocytes and granulocytes) were examined by flow cytometry. Differential leukocyte count was conducted using hematological analyzer. Results. Phagocytes from animals underwent of different protocols of placebo surgery, demonstrated various patterns of functional changes on day 29 after the manipulations. In animals from SO1 group, we observed signs of residual neuroinflammation (pro-inflammatory shift of microglia functional profile) along with ongoing resolution of systemic inflammation (anti-inflammatory metabolic shift of circulating phagocytes and peritoneal macrophages). In rats from SO2 group, pro-inflammatory polarized activation of peritoneal phagocytes was registered along with anti-inflammatory shift in microglia and circulating phagocytes. Conclusions. Sham surgery influences functions of phagocytic cells of different locations even in the far terms after the manipulations. These effects can be considered as combined long-term consequences of surgical brain injury and the use of anesthetics. Our observations evidences, that sham associated non-specific immunomodulatory effects should always be taken into consideration in animal models of inflammatory central nervous system diseases.

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Berge, Lillian Nordbø, Monika Østensen, and Arthur Revhaug. "Phagocytic cell activity in pre-eclampsia." Acta Obstetricia et Gynecologica Scandinavica 67, no. 6 (January 1988): 499–504. http://dx.doi.org/10.3109/00016348809029860.

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Gil-Lamaignere, C., A. Maloukou, J. L. Rodriguez-Tudela, and E. Roilides. "Human phagocytic cell responses toScedosporium prolificans." Medical Mycology 39, no. 2 (January 2001): 169–75. http://dx.doi.org/10.1080/mmy.39.2.169.175.

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31

Mege, J. L., C. Capo, B. Michel, J. L. Gastaut, and P. Bongrand. "Phagocytic cell function in aged subjects." Neurobiology of Aging 9 (January 1988): 217–20. http://dx.doi.org/10.1016/s0197-4580(88)80054-x.

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32

Etzioni, Amos. "Novel aspects of phagocytic cell disorders." Current Opinion in Allergy and Clinical Immunology 1, no. 6 (December 2001): 535–40. http://dx.doi.org/10.1097/00130832-200112000-00007.

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33

Ocon, P., J. M. Reguera, P. Morata, C. Juarez, A. Alonso, and J. D. Colmenero. "Phagocytic cell function in active brucellosis." Infection and Immunity 62, no. 3 (1994): 910–14. http://dx.doi.org/10.1128/iai.62.3.910-914.1994.

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34

Moschella, Samuel L., and Thomas G. Cropley. "Mononuclear phagocytic and dendritic cell systems." Journal of the American Academy of Dermatology 22, no. 6 (June 1990): 1091–97. http://dx.doi.org/10.1016/0190-9622(90)70158-e.

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35

Rezende, Gustavo L., Marcio Nakanishi, Shirley C. P. Couto, Carmen L. F. S. Martins, André L. L. Sampaio, Lucas F. F. Albuquerque, Selma A. S. Kückelhaus, and Maria I. Muniz-Junqueira. "Alterations in innate immune responses of patients with chronic rhinosinusitis related to cystic fibrosis." PLOS ONE 17, no. 5 (May 6, 2022): e0267986. http://dx.doi.org/10.1371/journal.pone.0267986.

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The role of phagocytes of children with cystic fibrosis (CF) associated with different phenotypes of chronic rhinosinusitis (CRS) is unclear. The aim of this study was to evaluate the phagocytic capacity of blood neutrophils and monocytes and production of superoxide anion by phagocytes in patients with CF with or without chronic rhinosinusitis and with or without nasal polyps (NP). This cross-sectional study was established in 2015–2017 in a tertiary reference center to the CF treatment, Brasilia, Brazil. Sample included 30 children volunteers with CRS related to CF (n = 16) and control subjects (n = 14). Epidemiological and clinical data were compared. Collection of 15 mL of peripheral blood and nasal endoscopy to identify the presence or absence of nasal polyps (NP) were performed. Phagocytosis of Saccharomyces cerevisiae by pathogen-associated molecular pattern receptors and opsonin receptors was assessed. Superoxide anion production was evaluated. The control group showed a higher phagocytic index to monocytes and neutrophils than to the CF or CF+CRS with NP groups [Kruskal-Wallis p = 0.0025] when phagocytosis were evaluated by pathogen-associated molecular pattern receptors (5 yeasts/cell). The phagocytic index of the CF+CRS without NP group was higher than in the CF+CRS with NP group (Kruskal-Wallis p = 0.0168). In the control group, the percentage of phagocytes involved in phagocytosis and superoxide anion production (74.0 ± 9.6%) were higher in all CF groups (p < 0,0001). The innate immune response, represented by phagocytic activity and superoxide anion production by monocytes and neutrophils was more impaired in patients with CF related or not related to CRS than in the control group. However, the phagocytic function of patients without NP showed less impairment.

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36

Greenberg, Steven. "Diversity in phagocytic signalling." Journal of Cell Science 114, no. 6 (March 15, 2001): 1039–40. http://dx.doi.org/10.1242/jcs.114.6.1039.

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Leslie, Mitch. "Rules of phagocytic attraction." Journal of Cell Biology 187, no. 5 (November 30, 2009): 584. http://dx.doi.org/10.1083/jcb.1875iti3.

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38

Shklyar, Boris, Flonia Levy-Adam, Ketty Mishnaevski, and Estee Kurant. "Caspase Activity Is Required for Engulfment of Apoptotic Cells." Molecular and Cellular Biology 33, no. 16 (June 10, 2013): 3191–201. http://dx.doi.org/10.1128/mcb.00233-13.

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Clearance of apoptotic cells by phagocytic neighbors is crucial for normal development of multicellular organisms. However, how phagocytes discriminate between healthy and dying cells remains poorly understood. We focus on glial phagocytosis of apoptotic neurons during development of theDrosophilacentral nervous system. We identified phosphatidylserine (PS) as a ligand on apoptotic cells for the phagocytic receptor Six Microns Under (SIMU) and report that PS alone is not sufficient for engulfment. Our data reveal that, additionally to PS exposure, caspase activity is required for clearance of apoptotic cells by phagocytes. Here we demonstrate that SIMU recognizes and binds PS on apoptotic cells through its N-terminal EMILIN (EMI), Nimrod 1 (NIM1), and NIM2 repeats, whereas the C-terminal NIM3 and NIM4 repeats control SIMU affinity to PS. Based on the structure-function analysis of SIMU, we discovered a novel mechanism of internal inhibition responsible for differential affinities of SIMU to its ligand which might prevent elimination of living cells exposing PS on their surfaces.

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Suresh, Madheswaran, Malarvizhi Gurusamy, and Natarajan Sudhakar. "MASKING ANTI-PHAGOCYTIC SIGNAL OF TUMOR BY PRO-PHAGOCYTIC SIGNAL-A KEY TO IMMUREMENT OF CANCER CELL." International Journal of Pharmacy and Pharmaceutical Sciences 8, no. 9 (September 1, 2016): 323. http://dx.doi.org/10.22159/ijpps.2016v8i9.12990.

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<p>Immune surveillance is a mechanism where cells and tissues are watched constantly by ever alerted immune system. Most incipient cancer cells are recognized and eliminated by the immune surveillance mechanism, but still tumors have the ability to evade immune surveillance and immunological killing. One greater arm that tumor use to evade immune surveillance, is by expressing anti-phagocytic signal (CD47). Here we present a provocative hypothesis where cancer cells are removed alive by phagocytic cell (DC). That in turn will elicit effective and higher immunogenic condition. All this could be possible by addition pro-phagocytic signal (PtdSer) over cancer cell surface (Breast Cancer), that mask the presence of anti-phagocytic signal (CD47). In other words, adding eat me signal (PtdSer) over the breast cancer cell surface that mask the presence of don’t eat me signal or anti-phagocytic signal present in breast cancer cell surface. This could be possible by using bi-specific antibody, conjugated to PEG-modified liposomes, which carry (PtdSer) pro-phagocytic signal (or) eat me signal, which target both CD47 and EGFRVIII on breast carcinoma. The simultaneous masking of anti-phagocytic signal, and adding of pro–phagocytic signal over cancer cell, will enhance the phagocytic clearance of live tumor cell and elicit immunological killing.</p>

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Somersan, Selin, and Nina Bhardwaj. "Tethering and tickling." Journal of Cell Biology 155, no. 4 (November 12, 2001): 501–4. http://dx.doi.org/10.1083/jcb.200110066.

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Several receptors are implicated in apoptotic cell (AC) uptake by phagocytic cells; however, their relative dominance in mammalian systems remains to be established. New studies shed light on the role of the phosphatidyl serine (PS) receptor (PSR). Ligation of PSR by PS on AC surfaces is considered essential for signaling uptake of ACs that are tethered to phagocytes via other receptors.

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Tsai, Wen-Hui, Shao-Chi Chang, Yu-Chieh Lin, and Hui-Chi Hsu. "CX3CL1(+) Microparticles-Induced MFG-E8 Enhances Apoptotic Cell Clearance by Alveolar Macrophages." Cells 10, no. 10 (September 28, 2021): 2583. http://dx.doi.org/10.3390/cells10102583.

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During the resolution phase of acute lung injury, apoptotic cells release CX3CL1 as a “find-me” signal to attract alveolar macrophage transmigration toward apoptotic cells for phagocytosis. However, it is still not clear whether CX3CL1 has pro-phagocytic activity on alveolar macrophage. In this study, we investigated the role of apoptotic NB4 cells-derived CX3CL1(+) microparticles (apo-MP) on the phagocytic activity of NR8383 cells. We demonstrate that exogenous CX3CL1 and apo-MP enhanced the phagocytic activity of NR8383 cells in a CX3 CR1-dependent manner. The apo-MP-enhanced phagocytic activity on NR8383 was attenuated when apo-MP and NR8383 cells were pre-treated with anti-CX3CL1 antibodies and anti-CX3CR1 antibody, respectively, before incubating both for phagocytic assay. Further studies demonstrate that exogenous CX3CL1 and apo-MP also enhanced NR8383 cells in their surface expression and release of MFG-E8 in a CX3CR1 dependent manner. The enhanced phagocytic activity of CX3CL1-treated NR8383 cells was attenuated when NR8383 cells were pre-treated with an anti-MFG-E8 antibody before CX3CL1 treatment. We conclude that apoptotic cell-derived CX3CL1(+) microparticles enhance the phagocytic activity of NR8383 cells by up-regulating their MFG-E8 as a bridge molecule, and these contribute to the formation of phagocytic synapses between apoptotic cells and alveolar macrophages for the subsequent phagocytic clearance of apoptotic cells.

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Sateriale, Adam, Archana Vaithilingam, Liam Donnelly, Peter Miller, and Christopher D. Huston. "Feed-Forward Regulation of Phagocytosis by Entamoeba histolytica." Infection and Immunity 80, no. 12 (October 8, 2012): 4456–62. http://dx.doi.org/10.1128/iai.00671-12.

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ABSTRACTThe parasitic protozoanEntamoeba histolyticais aptly named for its capacity to destroy host tissue. WhenE. histolyticatrophozoites invade the lamina propria of a host colon, extracellular matrices are degraded while host cells are killed and phagocytosed. The ability ofE. histolyticato phagocytose host cells correlates with virulencein vivo. In order to better understand the mechanism of phagocytosis, we used anE. histolyticaAffymetrix microarray chip to measure the total gene expression of phagocytic and nonphagocytic subpopulations. Using paramagnetic beads coated with a known host ligand that stimulates phagocytosis, phagocytic and nonphagocytic amoebae from a single culture were purified. Microarray analysis of the subpopulations identified 121 genes with >2-fold higher expression in phagocytic than in nonphagocytic amoebae. Functional annotation identified genes encoding proteins involved in actin binding and cytoskeletal organization as highly enriched gene clusters.Post hocanalyses of selected genes showed that the gene expression profile identified in the microarray experiment did not exist prior to cell sorting but rather was stimulated through phagocytosis. Further, these expression profiles correlated with an increase in phagocytic ability, asE. histolyticacultures exposed to an initial stimulus of phagocytosis showed increased phagocytic ability upon a second stimulus. To our knowledge, this is the first description of such feed-forward regulation of gene expression and phagocytic ability in a phagocyte.

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Schreiner, G. F. "The mesangial phagocyte and its regulation of contractile cell biology." Journal of the American Society of Nephrology 2, no. 10 (April 1992): S74. http://dx.doi.org/10.1681/asn.v210s74.

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The mesangium constitutes the core of the renal glomerulus. It consists of the matrix, composed of mucopolysaccharides and glycoproteins, and two cell types. The predominant cell type is the mesangial cell, resembling a vascular smooth muscle cell. Up to 15% of the mesangial cell population additionally consists of resident mesangial phagocytes. These are derived from the bone marrow and belong to the family of mononuclear leukocytes. They are phagocytic, express Fc and C3 receptors, and display membrane Ia antigens. They syngeneically stimulate lymphocyte proliferation via antigen presentation. They are equally potent allogeneic stimulating cells in mixed lymphocyte culture. The mesangium is also the preferred locus of the induced migration of monocytes in inflammatory and proteinuric states. The presence of both normally resident and inflammation-associated mesangial phagocyte is lipid dependent. Hyperlipidemia increases the population of mesangial phagocytes. Lipid restriction decreases their number and, as a result, diminishes the allogenicity of renal transplants and blunts the progression of glomerulonephritis. One signal regulating the infiltration of the mesangium by mononuclear phagocytes appears to be a complex neutral lipid that is highly and specifically chemotactic for monocytes. It is released by the contractile mesangial cell in response to the stimulation of its Fc receptor and to the mesangial deposition of macromolecules. Both resident and inflammatory mesangial phagocytes secrete factors that remodel the mesangial matrix, stimulate mesangial cell proliferation, alter glomerular basement membrane permeability, and regulate blood flow. The persistence of mononuclear phagocytes in an activated state within the mesangium contributes to the marked alteration in mesangial structure that eventuates in glomerulosclerosis in both immune and nonimmune models of glomerular injury.

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44

SkÖLd, C. M., A. Eklund, G. HalldÉN, and J. Hed. "Different cell surface and phagocytic properties in mononuclear phagocytes from blood and alveoli." APMIS 98, no. 1-6 (January 1990): 415–22. http://dx.doi.org/10.1111/j.1699-0463.1990.tb01052.x.

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45

Potoka, Douglas A., Sonshin Takao, Tetsuhiro Owaki, Gregory B. Bulkley, and Andrew S. Klein. "Endothelial Cells Potentiate Oxidant-Mediated Kupffer Cell Phagocytic Killing." Free Radical Biology and Medicine 24, no. 7-8 (May 1998): 1217–27. http://dx.doi.org/10.1016/s0891-5849(97)00453-x.

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46

Wendler, Astrid, Nicholas James, Michael H. Jones, and Christian Pernstich. "Phagocytosed Polyhedrin-Cytokine Cocrystal Nanoparticles Provide Sustained Secretion of Bioactive Cytokines from Macrophages." BioDesign Research 2021 (May 15, 2021): 1–12. http://dx.doi.org/10.34133/2021/9816485.

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Many cells possess the ability to engulf and incorporate particles by phagocytosis. This active process is characteristic of microorganisms as well as higher order species. In mammals, monocytes, macrophages, and microglia are among the so-called professional phagocytes. In addition, cells such as fibroblast and chondrocytes are classified as nonprofessional phagocytes. Professional phagocytes play important roles in both the innate and adaptive immune responses, wound healing, and tissue homeostasis. Consequently, these cells are increasingly studied as targets and vectors of therapeutic intervention to treat a range of diseases. Professional phagocytes are notoriously difficult to transfect limiting their study and manipulation. Consequently, efforts have shifted towards the development of nanoparticles to deliver a cargo to phagocytic cells via phagocytosis. However, this approach carries significant technical challenges, particularly for protein cargos. We have focused on the development of nanoscale cocrystalline protein depots, known as PODS®, that contain protein cargos, including cytokines. Here, we show that PODS are readily phagocytosed by nonprofessional as well as professional phagocytic cells and have attributes, such as highly sustained release of cargo, that suggest potential utility for the study and exploitation of phagocytic cells for drug delivery. Monocytes and macrophages that ingest PODS retain normal characteristics including a robust chemotactic response. Moreover, the PODS-cytokine cargo is secreted by the loaded cell at a level sufficient to modulate the behavior of surrounding nonphagocytic cells. The results presented here demonstrate the potential of PODS nanoparticles as a novel molecular tool for the study and manipulation of phagocytic cells and for the development of Trojan horse immunotherapy strategies to treat cancer and other diseases.

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47

Damisah, Eyiyemisi C., Robert A. Hill, Anupama Rai, Fuyi Chen, Carla V. Rothlin, Sourav Ghosh, and Jaime Grutzendler. "Astrocytes and microglia play orchestrated roles and respect phagocytic territories during neuronal corpse removal in vivo." Science Advances 6, no. 26 (June 2020): eaba3239. http://dx.doi.org/10.1126/sciadv.aba3239.

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Cell death is prevalent throughout life; however, the coordinated interactions and roles of phagocytes during corpse removal in the live brain are poorly understood. We developed photochemical and viral methodologies to induce death in single cells and combined this with intravital optical imaging. This approach allowed us to track multicellular phagocytic interactions with precise spatiotemporal resolution. Astrocytes and microglia engaged with dying neurons in an orchestrated and synchronized fashion. Each glial cell played specialized roles: Astrocyte processes rapidly polarized and engulfed numerous small dendritic apoptotic bodies, while microglia migrated and engulfed the soma and apical dendrites. The relative involvement and phagocytic specialization of each glial cell was plastic and controlled by the receptor tyrosine kinase Mertk. In aging, there was a marked delay in apoptotic cell removal. Thus, a precisely orchestrated response and cross-talk between glial cells during corpse removal may be critical for maintaining brain homeostasis.

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Gaforio, José Juan, Elena Ortega, Ignacio Algarra, María José Serrano, and Gerardo Alvarez de Cienfuegos. "NK Cells Mediate Increase of Phagocytic Activity but Not of Proinflammatory Cytokine (Interleukin-6 [IL-6], Tumor Necrosis Factor Alpha, and IL-12) Production Elicited in Splenic Macrophages by Tilorone Treatment of Mice during Acute Systemic Candidiasis." Clinical and Vaccine Immunology 9, no. 6 (November 2002): 1282–94. http://dx.doi.org/10.1128/cdli.9.6.1282-1294.2002.

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ABSTRACT The participation of NK cells in the activation of splenic macrophages or in resistance to systemic candidiasis is still a matter of debate. We had previously reported that there is a correlation between natural killer cell activation and resistance to systemic candidiasis. In those experiments we had used tilorone to boost NK cell activity in mice. Here we show a mechanism elicited by tilorone in splenic macrophages which could explain their effect on mouse survival during acute disseminated Candida albicans infection. The results demonstrate that tilorone treatment elicits, by a direct effect, the production of proinflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor alpha [TNF-α], and IL-12) by splenic macrophages. In addition, it increases the capacity of splenic macrophages to phagocytize C. albicans through activation of NK cells. We also demonstrate that the presence of NK cells is essential for maintaining a basal level of phagocytic activity, which characterizes splenic macrophages of naïve control mice. The results demonstrate that it is possible to identify two phenotypically and functionally peculiar cell populations among splenic macrophages: (i) cells of the “stimulator/secretor phenotype,” which show high levels of major histocompatibility complex (MHC) class II surface expression, are poorly phagocytic, and synthesize the proinflammatory cytokines IL-6, TNF-α, and IL-12, and (ii) cells of the “phagocytic phenotype,” which express low levels of MHC class II molecules, are highly phagocytic, and do not secrete proinflammatory cytokines.

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Molinari, Beatriz L., Deborah R. Tasat, Mónica A. Palmieri, and Rómulo L. Cabrini. "Kinetics of MTT-formazan exocytosis in phagocytic and non-phagocytic cells." Micron 36, no. 2 (February 2005): 177–83. http://dx.doi.org/10.1016/j.micron.2004.08.002.

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50

Plekhova, N. G., L. M. Somova, and E. I. Drobot. "The metabolism of the innate immunity cells in bacterial infections." Biomeditsinskaya Khimiya 61, no. 1 (January 2015): 105–14. http://dx.doi.org/10.18097/pbmc20156101105.

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Metabolic activity of innate immunity cells infected by various doses of Gram-negative (Yersinia pseudotuberculosis, Salmonella enteritidis) and Gram-positive (Staphylococcus aureus, Listeria monocytogenes) bacteria has been investigated. Using various animal models we found that during the initial period (up to 2 days) changes of infection in cellular responses depend on the type of the pathogen. In response to infection caused by Gram-negative bacteria predominant neutrophil accumulation in the foci of inflammation was observed, while Gram-positive bacteria induced preferential accumulation of macrophages. The study of metabolism of these cells showed that the response of terminally differentiated primed phagocytes to pathogen appearance was higher than in cells circulating in blood. In addition to the priming state the phagocyte reactivity is influenced by the bacterial load. At a low phagocyte/microbe ratio the cells reaction is almost undetectable, while an excess of microorganisms causes (despite of the increase of the phagocytic parameters) the hyperactivation of cell metabolism and production of maximal amounts of bactericide agents, which exhibit a damaging effect on the cell itself.

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