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Antimicrobial mechanisms in response to Mycobaterium leprae infection

  • Author(s): Dang, Angeline Tilly
  • Advisor(s): modlin, robert l
  • et al.
Abstract

The human body is constantly exposed to a myriad of bacterial organisms, and in

most cases, colonization of the host by these commensal bacteria is harmless and may even

be beneficial. However, a subset of bacteria are pathogenic causing debilitating health that

can lead to fatal diseases. Many microbes deploy strategies to evade and impair the host

response, further contributing to disease severity. In response to infectious agents, the host

can control and subvert infections by triggering both innate and adaptive immunity. The

microenvironment in which an infections occurs greatly dictates the strength, quality, and

duration of immune responses. Herein, we demonstrate mechanisms for triggering

protective immune responses during Mycobacterium leprae infection. Specifically, treatment

of 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 and

antigen presentation to T cells. Furthermore, T cells secrete elevated amounts of IFN-g

following antigenic activation, providing an amplification loop to further augment effective

host immunity. As M. leprae predominantly infect and reside in macrophages, we also

investigated mechanisms of macrophage activation. Our data reveals that treatment of M.

leprae-infected monocyte-derived-macrophages with IL-26, a T cell cytokine, results in

reduced viability of intracellular bacteria. IL-26 may have dual roles in antimycobacterial

defense, one which involves binding to bacterial bacilli and directly reducing its viability; and

the other involving activation of infected macrophages, increasing bacterial traffic to the

lysosomes, where they are degraded.

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