Open AccessMIR-181A-5P Attenuates Ovalbumin-Induced Allergic Inflammation in Nasal Epithelial Cells by Targeting IL-33/P38 MAPK Pathway
Author(s) -
Songliang Long,
Hua Zhang
Publication year - 2021
Publication title -
clinical and investigative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.391
H-Index - 47
eISSN - 1488-2353
pISSN - 0147-958X
DOI - 10.25011/cim.v44i4.37327
Subject(s) - ovalbumin , allergic inflammation , inflammation , p38 mitogen activated protein kinases , immunology , tumor necrosis factor alpha , cytokine , mapk/erk pathway , proinflammatory cytokine , pathogenesis , interleukin , medicine , chemistry , signal transduction , immune system , biochemistry
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.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.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.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.