Open AccessMycobacterium tuberculosis infection increases the number of osteoclasts and inhibits osteoclast apoptosis by regulating TNF‑α‑mediated osteoclast autophagy
Author(s) -
Wei Liu,
Juan Zhou,
Fangyong Niu,
Feifei Pu,
Zhiwei Wang,
Mi Huang,
Xiaolong Zhao,
Lin Yang,
Pengfei Tao,
Ping Xia,
Jing Feng
Publication year - 2020
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2020.8903
Subject(s) - osteoclast , autophagy , apoptosis , cell cycle , oncogene , tumor necrosis factor alpha , mycobacterium tuberculosis , molecular medicine , tuberculosis , cancer research , biology , microbiology and biotechnology , immunology , medicine , pathology , in vitro , genetics
Osteoarticular tuberculosis, a chronic inflammatory disease characterized by Mycobacterium tuberculosis ( M.tb ) infection, has become a serious problem in China. The present study was conducted to determine the mechanism of action of tumor necrosis factor (TNF)-α in the pathogenesis of osteoarticular tuberculosis. The number of osteoclasts in osteoarticular tuberculosis tissue samples was detected by tartrate-resistant acid phosphatase staining. Autophagy and apoptosis of osteoclasts were detected by western blotting, reverse transcription-quantitative PCR, transmission electron microscopy and TUNEL staining. The results showed that autophagy and the number of osteoclasts increased in the lesions of patients with osteoarticular tuberculosis compared with osteoarthritis samples. Moreover, activation of osteoclast autophagy inhibited the apoptosis of osteoclasts infected with M.tb , and increased the expression level of TNF-α. The results showed that TNF-α enhanced the autophagic activity of M.tb -infected osteoclasts and inhibited cell apoptosis. These findings indicated that M.tb infection induced osteoclast production and inhibited osteoclast apoptosis by regulating TNF-α-mediated osteoclast autophagy, revealing a new mechanism for TNF-α in the pathogenesis of osteoarticular tuberculosis.