The role of B-1 cells in experimental infection with Encephalitozoon cuniculi in mice

Abstract

Encephalitozoon species of microsporidia infect a wide range of mammals and are known causes of opportunistic infections in persons with AIDS and other immune deficiencies. In animals cause disseminated infections and death, causing huge economic losses when they reach herds of rabbits. The adaptive immunity is clearly essential for clearance of these parasites evidence is mounting that the response initiated by the innate arm of immunity may ultimately define whether or not the parasite can survive. Current research has focused on elucidating the mechanisms of resistance and susceptibility. The cells known as B-1 B lymphocytes are specialized, located in the peritoneal and pleural cavities, and act as antigen presenters, phagocytes, produce and use IL-10 as a potent negative regulator of cell-mediated immunity, among other functions. The possible role of these cells and their secreted products in the dynamics of inflammation of various etiologies is totally unknown. It has been demonstrated that B-1 cells are a major source of IL-10, a known anti-inflammatory mediator that has a regulatory function of macrophages. The goal of this project is to evaluate the role of B-1 cells in experimental infection with E. cuniculi in BALB/c. BALB/c and BALB/c Xid mice, submitted or not to immunosuppression with cyclophosphamide, will be inoculated with spores of E. cuniculi. The spores are cultured MDCK cell lineage. The animals will be euthanized and samples of blood, peritoneal fluid, spleen and liver will be collected to carry out phenotyping of CD8+ T cells, CD4+ T cells, NKT cells, NK cells and B-1, by flow cytometry. Additionally, the cytokine profile of Th1 and Th2 cells will be quantitated by flow cytometry by CBA assay and quantification of IL-10 will be done by ELISA. Statistical comparisons are made using analysis of variance (ANOVA) and Tukey and Kramer, with significance values less than P < 0.05 (AU)