Papel de células B-1 sobre atividade de células fagocíticas em infecção por Encephalitozoon cuniculi

Resumo (EN)

Microsporidia are obligate intracellular fungal pathogens that infect a wide range of hosts in the animal kingdom. Encephalitozoon cuniculi was the first mammalian microsporidian successfully grown in vitro and infects macrophages, epithelial and endothelial cells and fibroblasts in a variety of mammals, including rodents, monkeys, carnivores, rabbits and humans. There are limited data on the host responses to these opportunistic pathogens and one study in vivo from our group describing B-1 cell involving in the decrease of susceptibility of mice to the E. cuniculi infection. To understand the role of B-1 cells in this issue we performed macrophages response to E. cuniculi in the presence or absence of B-1 cells. Adherent peritoneal cells from BALB/c (BALB/c APerC) and B-1 cell-deficient XID (XID APerC) mice and B-1 Cell-Derived Phagocyte (B-1 CDP) were simultaneously infected with E. cuniculi. The examination by light and transmission electronic microscopy demonstrated differences between BALB/c and XID APerC. Samples of BALB/C APerC after 1h and 48h revealed a large amount of lymphocytes in addition to macrophages and spores of E. cuniculi in great quantity outside the cells. In XID APerC samples the predominance were macrophages with a higher number of phagocytic cells with spores inside of cells. Also, an increased in IL-6, IL-10 and MCP-1 levels were observed in XID APerC. 96h and 144h in BALB/c APerC revealed a low cellularity with a great quantity of spores outside de cells indicating degeneration and death of phagocytes. Increased levels of MCP-1, TNF and IL-6 were detected in infected group in these cultures. Contrary, in XID APerC we observed a higher number of intact phagocytic cells with spores in degeneration and an increased TNF and NO production in infected group compared to control group. The findings suggest B-1 cells interfere with macrophage activity, increasing the microbicidal activity of macrophages and modulating cytokines secretion.