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MIR-181A-5P Attenuates Ovalbumin-Induced Allergic Inflammation in Nasal Epithelial Cells by Targeting IL-33/P38 MAPK
1Department of Otorhinolaryngology, Hunan Children's Hospital, Changsha, China. email@email.com.
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.
Insights
MicroRNA miR-181a-5p is downregulated in allergic rhinitis (AR). Restoring miR-181a-5p suppresses inflammation by inhibiting the IL-33/p38 MAPK pathway, suggesting a therapeutic role in AR.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Chronic inflammation of nasal tissues is key in allergic rhinitis (AR) pathogenesis.
- MicroRNAs (miRNAs) are implicated in allergic inflammation, but their specific role in AR is unclear.
- Understanding miRNA function is crucial for developing novel AR therapies.
Purpose of the Study:
- To investigate the functional role of miR-181a-5p in allergic rhinitis.
- To elucidate the molecular mechanism underlying miR-181a-5p's action in AR.
- To determine if miR-181a-5p has anti-inflammatory properties in AR.
Main Methods:
- Induced allergic inflammation in RPMI2650 cells using ovalbumin.
- Assessed anti-inflammatory effects by measuring pro-inflammatory cytokines (IL-1β, IL-6, TNF-α).
- Employed quantitative real-time PCR, ELISA, luciferase assays, and gain-of-function assays to study miR-181a-5p and the IL-33/p38 MAPK axis.
Main Results:
- miR-181a-5p was significantly downregulated in AR patient tissues and ovalbumin-treated cells.
- Overexpressing miR-181a-5p suppressed inflammatory cytokine production.
- miR-181a-5p directly targeted and downregulated IL-33, inhibiting the p38 MAPK signaling pathway.
Conclusions:
- miR-181a-5p restricts allergic inflammation by inhibiting the IL-33/p38 MAPK pathway.
- miR-181a-5p demonstrates a significant anti-inflammatory role in allergic rhinitis.
- This miRNA represents a potential therapeutic target for AR treatment.
