Harnessing of TLR-mediated autophagy to combat mycobacteria in macrophages

Yi Xu, Elmoataz Abdel Fattah, Xian De Liu, Chinnaswamy Jagannath, N. Tony Eissa

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)S33-S37
Issue numberSUPPL.
StatePublished - Dec 1 2013


  • Autophagy
  • LPS
  • Mycobacteria tuberculosis
  • Receptors
  • Toll-like

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases


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