Immune regulation of miR-30 on the -induced TLR/MyD88 signaling pathway in THP-1 cells.

The present study aimed to examine the expression of microRNA (miR)-30 family members in THP-1 human monocytes cells during (MTB) H37Rv infection, and to investigate the role of miR-30 in the regulation of MTB-induced Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) activation and cytokine expression. The THP-1 cells were infected with MTB H37Rv and the expression of miR-30 family members was determined by reverse transcription-quantitative polymerase chain reaction analysis. In addition, miR-30a and miR-30e mimics were transfected into THP-1 cells to overexpress miR-30a and miR-30e. The expression of TLR2, TLR4 and MyD88 was determined by western blot analysis, and the expression of the cytokines tumor necrosis factor-α, interleukin (IL)-6, and IL-8 was determined using ELISA assays. A luciferase reporter assay was used to identify the target gene of miR-30a. MTB infection was demonstrated to significantly induce miR-30a and miR-30e expression in THP-1 cells in a time-dependent manner. Forced overexpression of miR-30a, but not miR-30e, exhibited an inhibitory effect on TLR/MyD88 activation and cytokine expression in the uninfected and MTB-infected THP-1 cells. The luciferase reporter assay demonstrated that miR-30a directly regulates the transcriptional activity of the MyD88 3'-untranslated region. In conclusion, the present study, to the best of our knowledge, is the first to demonstrate that miR-30a suppresses TLR/MyD88 activation and cytokine expression in THP-1 cells during MTB H37Rv infection, and that MyD88 is a direct target of miR-30a. The current study may aid in the development of novel therapeutic approaches for treating MTB.