Harnessing of TLR-mediated autophagy to combat mycobacteria in macrophages. Academic Article uri icon

Overview

abstract

  • Autophagy, an evolutionary highly conserved process in virtually all eukaryotic cells, involves the sequestration of cytosol regions within double-membrane bound compartments and delivery of the contents to the lysosomes for degradation. Rapidly accumulating evidence has shown that autophagy is a component of innate immunity and is involved in host defense elimination of pathogens. Our previous studies show that Toll-like receptor 4 (TLR4) is a sensor for autophagy associated with innate immunity. We, now, further demonstrate that LPS or poly(I:C)-treatment significantly reduced mycobacterial viability in mouse macrophages. In addition, LPS reduction of mycobacterial viability was abrogated with the use of autophagy inhibitor 3-MA and in autophagy deficient macrophages. These findings demonstrate that TLR3 or TLR4 stimulation induces autophagy-mediated elimination of mycobacteria in macrophages. These results provide groundwork for therapeutic strategies directed at elimination of mycobacterial infections in macrophages.

publication date

  • December 1, 2013

Research

keywords

  • Autophagy
  • Immunity, Cellular
  • Immunity, Innate
  • Macrophages
  • Mycobacterium Infections
  • Mycobacterium tuberculosis

Identity

Scopus Document Identifier

  • 84891600583

Digital Object Identifier (DOI)

  • 10.1016/S1472-9792(13)70008-8

PubMed ID

  • 24388647

Additional Document Info

volume

  • 93 Suppl