Influence of normal microbiota on some aspects of the immune response during experimental infection with Trypanosoma cruzi in mice

Abstract

To study the influence of normal associated microbiota on systemic immunological responses during experimental Chagas' disease, germ-free and conventional NIH Swiss mice were infected with Y strain of Trypanosoma cruzi. Although no statistical differences in mortality and parasitaemia were found, conventional mice showed IFN-ª, TNF-AE and NO production (P , 0 . 05) by spleen cell cultures and higher blood levels of immunoglobulins of the IgG2a isotype (P , 0 . 05) when compared to their germ-free counterparts. Moreover, higher levels of IgG1 were also found in conventional animals. On the other hand, no differences in IL10 production were found between germ-free and conventional mice after infection (P , 0 . 05). Interestingly, spleen cell cultures from non-infected germ-free mice spontaneously produced higher levels of IL10 than cultures from conventional mice. Moreover, cultures from non-infected germ-free mice responded to T. cruzi antigens with IFN-ª production, contrary to cultures from conventional animals. In conclusion, the presence of the normal microbiota skews the immune response towards production of inflammatory cytokines during experimental infection with T. cruzi in mice. However, the increase in production of cytokines that is linked to resistance to this parasite did not alter the outcome of infection significantly, probably due to high virulence of the Y strain.

Transient TLR Activation Restores Inflammatory Response and Ability To Control Pulmonary Bacterial Infection in Germfree Mice

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Gut microbiome and anticancer immune response: really hot Sh*t!

“…First, colonization by commensal microorganisms is key to immune development. [9][10][11][12] Second, the commensal community keeps in check invading pathogens and prevents them from expressing virulence. 13,14 Third, the intestinal microbiota appears to digest glycans and regulate fat storage in mice and potentially in humans.…”

Early Innate Immunity to Bacterial Infection in the Lung Is Regulated Systemically by the Commensal Microbiota via Nod-Like Receptor Ligands

“…Their importance has been demonstrated in numerous clinical studies and by using animal models, which show that disruption of host-commensal interactions is associated with a variety of diseases and conditions (1,2,(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). These include cancer (8), chronic intestinal inflammation (12,15), autoimmunity (14), and increased susceptibility to infection by bacteria, viruses, and parasites, both in the intestine and at extraintestinal sites (1,4,(16)(17)(18)(19)(20)(21)(22)(23)(24). An underlying principal emerging from these studies is that the commensal microbiota is a major regulator of host immune function, and it is the disruption of this interaction that underlies many of these conditions.…”