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      Harnessing of TLR-mediated autophagy to combat mycobacteria in macrophages.

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          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.

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          Author and article information

          Journal
          Tuberculosis (Edinb)
          Tuberculosis (Edinburgh, Scotland)
          Elsevier BV
          1873-281X
          1472-9792
          Dec 2013
          : 93 Suppl
          Affiliations
          [1 ] Department of Medicine, Baylor College of Medicine, University of Houston Medical School, Houston, TX, USA.
          [2 ] Pathology & Laboratory Medicine Department, University of Houston Medical School, Houston, TX, USA.
          [3 ] Department of Medicine, Baylor College of Medicine, University of Houston Medical School, Houston, TX, USA. Electronic address: teissa@bcm.edu.
          Article
          S1472-9792(13)70008-8
          10.1016/S1472-9792(13)70008-8
          24388647
          0387fcc0-5a44-4ae8-ab26-c11141204a72
          History

          Autophagy,LPS,Mycobacteria tuberculosis,Toll-like Receptors

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