Journal
CELL HOST & MICROBE
Volume 17, Issue 3, Pages 345-356Publisher
CELL PRESS
DOI: 10.1016/j.chom.2015.01.007
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Funding
- Department of Biotechnology, Government of India, through the SyS TB network programme
- Council of Scientific and Industrial Research (CSIR), Government of India
- CSIR
- University Grants Commission, Government of India
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The outcome of the interaction between Mycobacterium tuberculosis (Mtb) and a macrophage depends on the interplay between host defense and bacterial immune subversion mechanisms. MicroRNAs critically regulate several host defense mechanisms, but their role in the Mtb-macrophage interplay remains unclear. MicroRNA profiling of Mtb-infected macrophages revealed the downregulation of miR-let-7f in a manner dependent on the Mtb secreted effector ESAT-6. We establish that let-7f targets A20, a feedback inhibitor of the NF-kappa B pathway. Expression of let-7f decreases and A20 increases with progression of Mtb infection in mice. Mtb survival is attenuated in A20-deficient macrophages, and the production of TNF, IL-1 beta, and nitrite, which are mediators of immunity to Mtb, is correspondingly increased. Further, let-7f overexpression diminishes Mtb survival and augments the production of cytokines including TNF and IL-1 beta. These results uncover a role for let-7f and its target A20 in regulating immune responses to Mtb and controlling bacterial burden.
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