Immune regulation of miR‑30 on the Mycobacterium tuberculosis‑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 Mycobacterium tuberculosis (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.