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Antimicrobial mechanisms in response to Mycobaterium leprae infection

The human body is constantly exposed to a myriad of bacterial organisms, and inmost cases, colonization of the host by these commensal bacteria is harmless and may evenbe beneficial. However, a subset of bacteria are pathogenic causing debilitating health thatcan lead to fatal diseases. Many microbes deploy strategies to evade and impair the hostresponse, further contributing to disease severity. In response to infectious agents, the hostcan control and subvert infections by triggering both innate and adaptive immunity. Themicroenvironment in which an infections occurs greatly dictates the strength, quality, andduration of immune responses. Herein, we demonstrate mechanisms for triggeringprotective immune responses during Mycobacterium leprae infection. Specifically, treatmentof M. leprae-infected CD1a+ Langerhans cells, a dendritic cells subset localized in the skin and mucosa, with IFN-g induces autophagy, leading to increased antimicrobial activity andantigen presentation to T cells. Furthermore, T cells secrete elevated amounts of IFN-gfollowing antigenic activation, providing an amplification loop to further augment effectivehost immunity. As M. leprae predominantly infect and reside in macrophages, we alsoinvestigated mechanisms of macrophage activation. Our data reveals that treatment of M.leprae-infected monocyte-derived-macrophages with IL-26, a T cell cytokine, results inreduced viability of intracellular bacteria. IL-26 may have dual roles in antimycobacterialdefense, one which involves binding to bacterial bacilli and directly reducing its viability; andthe other involving activation of infected macrophages, increasing bacterial traffic to thelysosomes, where they are degraded.