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.
Original language | English (US) |
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Pages (from-to) | S33-S37 |
Journal | Tuberculosis |
Volume | 93 |
Issue number | SUPPL. |
DOIs | |
State | Published - Dec 1 2013 |
Keywords
- Autophagy
- LPS
- Mycobacteria tuberculosis
- Receptors
- Toll-like
ASJC Scopus subject areas
- Microbiology
- Immunology
- Microbiology (medical)
- Infectious Diseases