bioRxivMicrobiology
B-1 cell-mediated modulation of M1-macrophage profile can ameliorate microbicidal functions and disrupt the evasion mechanisms of Encephalitozoon cuniculi
A. Pereira, A. M. Alvares-Saraiva, F. T. d. C. Konno, D. D. Spadacci-Morena, E. C. Perez, M. Mariano, M. A. Lallo
Abstract
Here, we have investigated the possible effect of B-1 cells on the activity of peritoneal macrophages in E. cuniculi infection. In the presence of B-1 cells, peritoneal macrophages had an M1 profile with showed increased phagocytic capacity and index, associated with the intense microbicidal activity, increased proinflammatory cytokines production and a higher percentage of apoptotic death. The absence of B-1 cells was associated with a predominance of the M2 macrophages, indicating reduced phagocytic capacity and index, microbicidal activity, proinflammatory cytokine production, and apoptotic death, but equal death rate. In addition, in the M2 macrophages, spores of phagocytic E. cuniculi with polar tubular extrusion were observed, which is an important mechanism of evasion of the immune response. The results showed the importance of B-1 cells in the modulation of macrophage function against E. cuniculi infection, increasing microbicidal activity, and reducing the fungal mechanisms involved in the evasion of the immune response.\n\nHighlightsO_LIE. cuniculi phagocytosis and microbicidal activity by macrophages increases in the presence of B-1 cells\nC_LIO_LIM1 macrophage profiles were predominant in the presence of B-1 cells\nC_LIO_LIExtrusion of the polar tubule of E. cuniculi occur inside M2 macrophages in cultures without B-1 cells\nC_LIO_LIB-1 cells derived phagocytes (B-1CDP) identified with microbicidal activity against spores of E. cuniculi\nC_LI\n\nAuthor SummaryThe adaptive immune response plays a key role against Encephalitozoon cuniculi, an opportunistic fungus for T cells immunodeficient patients. The role of B cells and antibody play in natural resistance to Encephalitozoon cuniculi remains unresolved. Previously, we demonstrated that B-1 deficient mice (XID), an important component of innate immunity, were more susceptible to encephalitozoonosis, despite the increase in the number of CD4+ and CD8+ T lymphocytes. Here we observed that the absence of B-1 cells was associated with a larger population of M2 macrophages, an anti-inflammatory profile, which had lower microbicidal activity and phagocytic E. cuniculi spores were seen with the extrusion of the polar tubule, which is an important mechanism of evasion of the immune response. The results showed the importance of B-1 cells in the modulation of macrophage function against E. cuniculi infection, increasing microbicidal activity, and reducing the fungal mechanisms involved in the evasion of the immune response.
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