科研之友
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摘要
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.
Methodology/Principal Findings: 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-alpha, IL-1 beta, 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-kappa B signaling pathway cascades. Consistent with the anti-inflammation effect, a higher bacterial burden was seen in miR-146a mimics-treated macrophages.
Conclusion/Significance: Here, we demonstrated that mycobacteria-induced miR-146a could modulate inflammatory response by targeting IRAK1 and TRAF6 and facilitate mycobacteria replication in macrophages.
