Tuberculosis (TB), caused by Mycobacterium tuberculosis, has led to many clinical disorders and remains a major global health problem, leading to great morbidity and mortality worldwide. Previous studies reported that Mycobacterium tuberculosis (M.tb) has evolved to utilize various mechanisms to evade or attenuate the immune response, such as dysregulation of miRNAs. However, reports concerning the role of miRNAs in M.tb infection are limited. Here, we report that a host microRNA, miR-26b, was significantly down-regulated by M.tb infection in THP-1 cells. Subsequently, our results of in vitro experiments demonstrate that miR-26b is a negative regulator of the NF-κB pathway by directly targeting TAK1, resulting in the inhibition of immune response, and promotion of M.tb replication and gene expression. Taken together, our findings provide detailed molecular mechanisms for how miR-26 inhibits inflammatory cytokine secretion during M.tb infection in THP-1 cells, and these results suggest anti-M.tb as a promising therapy.
Keywords: Mycobacterium tuberculosis; NF-κB; TAK1; miR-26b.
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