title: MicroRNA-146a represses mycobacteria-induced inflammatory response and facilitates bacterial replication via targeting IRAK-1 and TRAF-6.
abstract: BACKGROUND
  Apart from triggering host immune responses, macrophages also act as a major reservoir for mycobacteria. For better survival, mycobacteria have evolved various mechanisms to modulate the production of proinflammatory cytokines in macrophages, and manipulation of micro-RNA (miRNA) expression has been considered as an important one.
  
  
  RESULTS
  In this study, we found that miR-146a expression was significantly increased in a time- and dose-dependent manner in mycobacteria-infected macrophages. It could obviously reduce the induction of proinflammatory cytokines TNF-α, IL-1β, IL-6 and chemokine MCP-1 by targeting interleukin-1 receptor-associated kinase-1 (IRAK-1) and TNF receptor-associated factor-6 (TRAF-6), two key elements involved in the TLR/NF-κB signaling pathway cascades. Consistent with the anti-inflammation effect, a higher bacterial burden was seen in miR-146a mimics-treated macrophages.
  
  
  CONCLUSIONS
  Here, we demonstrated that mycobacteria-induced miR-146a could modulate inflammatory response by targeting IRAK1 and TRAF6 and facilitate mycobacteria replication in macrophages.
authors.affiliation: Institute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China.
authors.forename: Shuo
authors.initials: S
authors.lastname: Li
authors.affiliation: Jiangsu Provincial Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People's Republic of China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Yue
authors.affiliation: Jiangsu Provincial Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People's Republic of China.
authors.forename: Wei
authors.initials: W
authors.lastname: Xu
authors.affiliation: Institute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China ; Jiangsu Provincial Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People's Republic of China.
authors.forename: Sidong
authors.initials: S
authors.lastname: Xiong
mesh_terms: D000818:Animals; D007249:Inflammation / Q000378:metabolism* / Q000382:microbiology; D053592:Interleukin-1 Receptor-Associated Kinases / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism* / Q000382:microbiology; D051379:Mice; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000378:metabolism*; D009161:Mycobacterium; D015398:Signal Transduction / Q000502:physiology; D048029:TNF Receptor-Associated Factor 6 / Q000378:metabolism*
chemical_list: D035683:MicroRNAs; C534190:Mirn146 microRNA, mouse; D048029:TNF Receptor-Associated Factor 6; D053592:Interleukin-1 Receptor-Associated Kinases