Mycobacterium tuberculosis Rv0927c Inhibits NF-κB Pathway by Downregulating the Phosphorylation Level of IκBα and Enhances Mycobacterial Survival
Aihong Xia, Xin Li, Juanjuan Quan, Xiang Chen, Zhengzhong Xu, Xinan Jiao
Frontiers in Immunology · 2021-08
Abstract
Through long-term coevolution with its host, Mycobacterium tuberculosis ( M. tuberculosis ) uses multiple strategies to escape host defenses. The M. tuberculosis Rv0927c protein is predicted to be a short-chain dehydrogenase/reductase related to bacterial metabolism. However, the role of Rv0927c during M. tuberculosis infection remains unclear. Here, we observed that Rv0927c inhibited the expression of IL-6, TNF-α, and IL-1β, an effect dependent on NF-κB and p38 pathways. Western blot analysis of macrophages infected with recombinant Mycobacterium smegmatis strains showed that Rv0927c attenuated NF-κB activation by downregulating the phosphorylation of IκBα. Additionally, Rv0927c enhanced intracellular survival of M. smegmatis and pathological effects in mice. In conclusion, our findings demonstrate that Rv0927c functions as a regulator of inflammatory genes and enhances the survival of M. smegmatis .
MeSH terms
- Mycobacterium smegmatis
- Mycobacterium tuberculosis
- Western blot
- Tuberculosis
- Phosphorylation
- Microbiology
- Biology
- Intracellular
- NF-κB
- Mycobacterium
- Gene