Autophagy during Mycobacterium tuberculosis infection and implications for future tuberculosis medications |
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Authors: | Xiaowen Yu Chunmei Li Weiling Hong Weihua Pan Jianping Xie |
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Affiliation: | 1. Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University, Beibei, Chongqing 400715, P.R. China;2. Department of Microbiology and Molecular Genetics, Department of Dermatology, Changzheng Hospital, Institute of Medical Mycology, Shanghai Key Laboratory of Molecular Medical Mycology, Second Military Medical University, Shanghai, P.R. China |
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Abstract: | Autophagy is a cellular homeostasis mechanism to eliminate unwanted or excessive organelles, or for the turnover of long-life cytosolic macromolecules. During Mycobacterium tuberculosis infection, autophagy represents not only an antimicrobial mechanism for the clearance of the intracellular pathogen, but also prevents excessive inflammation, avoiding the adverse effects on host. Here we focus on the anti-tuberculosis autophagy and signal pathways involved, and attempt to depict an integrative map of the interaction between autophagy and cytokine, ROS production, vitamin D, and inflammatory response. Novel autophagy-based therapy is also summarized. This integrative insight might add some novel thoughts for better tuberculosis medications. |
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