MicroRNA-155-5p modulates the progression of acute respiratory distress syndrome by targeting interleukin receptors.

Acute respiratory distress syndrome (ARDS) is a multifactorial inflammatory lung failure with a high incidence and a high cost burden. However, the underlying pathogenesis of ARDS is still unclear. Recently, microRNA has been shown to have critical function in regulating the pathogenesis of ARDS development and inflammation. To identify the important microRNA in the serum from patients with ARDS that may be potential biomarkers for the disease and explore the underlying disease mechanism. We found significant upregulation of miR-155-5p expression in serum samples from patients with ARDS compared with the control group (p < 0.01). The levels of interleukin receptors and inflammatory cytokines were significantly increased in blood samples from patients with ARDS (p < 0.05). In the cell model, miR-155-5p had a binding site in the 3'-UTR of the three interleukin receptors. In LPS-simulated BEAS-2B cells, transfection of miR-155-5p mimic inhibited the expression levels of these interleukin receptors, and was found to directly target the inflammatory response of leukocyte nodulin receptor through NF-kB signaling. In conclusion, miR-155-5p can alleviate LPS-simulated injury that induces the expression of IL17RB, IL18R1, and IL22RA2 by affecting the NF-kB pathway; however, it cannot change the occurrence of inflammatory storms. Collectively, this suggests that the progression of ARDS is the result of effects of the multiple regulatory pathways, providing novel evidence for the therapy of ARDS.