Lack of host gut microbiota alters immune responses and intestinal granuloma formation during schistosomiasis.

摘要: Fatalities from schistosome infections arise due to granulomatous, immune-mediated responses eggs that become trapped in host tissues. Schistosome-specific immune are characterized by initial T helper type 1 (Th1) and our previous studies demonstrated myeloid differentiation primary response gene 88 (Myd88)-deficient mice failed initiate such vivo. Paradoxically, schistosomal antigens fail stimulate innate cells release proinflammatory cytokines vitro. Since Schistosoma mansoni infection is an intestinal disease, we hypothesized commensal bacteria could act as bystander activators of the system instigate Th1 responses. Using a broad spectrum orally administered antibiotics anti-mycotics analysed schistosome-infected were simultaneously depleted gut bacteria. After depletion there was significantly less inflammation intestine, which accompanied decreased granuloma development. In contrast, liver pathology remained unaltered. addition, schistosome-specific skewed faecal egg excretion diminished. This study demonstrates microbiota can third partner instigating helminth-specific