Long noncoding RNA MALAT1 regulates sepsis in patients with burns by modulating miR-214 with TLR5

The present study aimed to identify the involvement of the dysregulation of the metastasis-associated lung adenocarcinoma transcript-1 (MALAT1)/microRNA (miR)-214/Toll-like receptor (TLR)5 signaling pathway in the development of post-burn sepsis. THP-1 cells were used in the present study, in addition to 8-10 week-old mice. ELISA analysis was performed to examine the expression levels of inflammation-associated factors. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis and western blotting were performed to analyze the influence of burns or burns with infection on the production of MALAT1, miR-214 and TLR5. Commonly-used software and a luciferase assay was used to confirm the target gene of miR-214. RT-qPCR analysis and western blotting were performed to elucidate the effects of lipopolysaccharide (LPS), miR-214 and MALAT1 on the expression of miR-214, TLR5, tumor necrosis factor (TNF)-, interleukin (IL)-6 and IL-10. Burn injury increased TLR5, TNF-, IL-6 and IL-10 expression levels, which were abolished by treatment with MALAT1. miR-214 directly targeted TLR5 by binding to the TLR5 3 untranslated region (ITR), and the luciferase activity of the wild-type, and not the mutant, TLR5 3UTR was reduced following transfection with miR-214. In cells not treated with LPS, MALAT1 and anti-miR-214 significantly enhanced TLR5, TNF-, IL-6 and IL-10 expression, and repressed miR-214 production; whereas, miR-214 and MALAT1 short hairpin (sh)RNA decreased TLR5, TNF-, IL-6 and IL-10 expression levels, and increased miR-214 expression. In cells treated with LPS, LPS reduced miR-214 expression and increased TLR5, TNF-, IL-6 and IL-10 expression compared with LPS-untreated cells, and the effects of MALAT1, anti-miR-214, miR-214 and MALAT1 shRNA on TLR5, TNF-, IL-6 and IL-10 were the same as in LPS-untreated cell. The results of the present study indicated the association between the dysregulation of MALAT1/miR-214/TLR5 and the risk of post-burn sepsis.