Conclusion
The results suggest that miR-181a-5p restricted allergic inflammation through inhibition of IL-33/p38 MAPK pathway, indicating miR-181a-5p may play an anti-inflammatory role in AR.
Methods
Allergic inflammatory reaction was induced by ovalbumin in human nasal epithelial cell line RPMI2650. The anti-inflammatory effects of miR-181a-5p were evaluated by examining pro-inflammatory cytokines (interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α)) in the culture of RPMI-2650 cells stimulated by ovalbumin, using quantitative real-time reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Luciferase assay and gain-of-function assay were used to investigate the association of miR-181a-5p and IL-33/p38 MAPK axis.
Purpose
Chronic inflammation of the nasal mucosal tissues plays an important role in the pathogenesis of allergic rhinitis (AR). Aberrantly-expressed micro ribonucleic acid (miRNA) has been found to have strong associations with the inflammatory reactions in allergic diseases; however, its functional significance and molecular mechanism in AR remains unclear. The purpose of this study is to determine the functional role and mechanism of miR-181a-5p in AR.
Results
MiR-181a-5p was significantly downregulated in mucosal tissues of AR patients and in RPMI-2650 cells treated with ovalbumin. The overexpression of miR-181a-5p showed prominent suppression of inflammatory cytokine production in RPMI-2650 cells with the stimulation of ovalbumin. MiR-181a-5p directly targeted, and negatively regulated IL-33 to suppress the activation of p38 MAPK signalling.