Journal
TUBERCULOSIS
Volume 93, Issue -, Pages S33-S37Publisher
CHURCHILL LIVINGSTONE
DOI: 10.1016/S1472-9792(13)70008-8
Keywords
Autophagy; Toll-like Receptors; Mycobacteria tuberculosis; LPS
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Funding
- NHLBI NIH HHS [R01 HL069033, R01 HL080205] Funding Source: Medline
- NIAID NIH HHS [P30 AI036211] Funding Source: Medline
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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. (C) 2013 Elsevier Ltd. All rights reserved.
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