MicroRNA‑124‑3p attenuates severe community‑acquired pneumonia progression in macrophages by targeting tumor necrosis factor receptor‑associated factor 6.

Community‑acquired pneumonia (CAP) is a severe type of pneumonia in adults, with a high mortality rate. Macrophages have been reported to mediate severe CAP (SCAP) in vitro following administration of LPS. Therefore, the present study established a SCAP model in Ana‑1 macrophages by lipopolysaccharide (LPS) induction, and aimed to explore the function of microRNA (miR)‑124‑3p in the LPS‑induced SCAP. The effect of LPS on Ana‑1 cell viability was evaluated by an MTT assay. In addition, the protein and mRNA levels of interleukin (IL)‑1β and tumor necrosis factor (TNF)‑α were determined by enzyme‑linked immunosorbent assay and reverse transcription‑quantitative polymerase chain reaction, respectively. The nuclear factor (NF)‑κB activity and phosphorylation of p38 mitogen‑activated protein kinase (MAPK) were also evaluated by western blotting. The results demonstrated that exposure to 0.1 µg/ml LPS displayed no evident toxicity on macrophages. Compared with the control group, higher TNF receptor‑associated factor 6 (TRAF6) mRNA and protein levels were observed subsequent to induction by LPS (0.1 µg/ml), suggesting the promoting role of TRAF6 in SCAP. Furthermore, miR‑124‑3p was proven to target the 3'‑untranslated region (3'UTR) of TRAF6. The miR‑124‑3p mimic effectively inhibited the LPS‑induced upregulation of IL‑1β and TNF‑α secretion, and mRNA expression levels in macrophages, which may be mediated by the p38 MAPK and NF‑κB signaling pathway. Taken together, these results strongly indicated that miR‑124‑3p targeted the 3'UTR of TRAF6, while it attenuated SCAP by reducing LPS‑induced inflammatory cytokine production and inhibiting the activation of p38 MAPK and NF‑κB signaling pathways. These findings indicate the immunoregulatory role of miR‑124‑3p against macrophage‑mediated SCAP.