AI Article Synopsis
- Trim31 is identified as a significant factor in airway inflammation related to asthma, with its expression notably reduced in the lungs of asthmatic mice.
- Mice lacking Trim31 exhibited more severe inflammation and tissue damage after being induced with ovalbumin (OVA), highlighting its role in regulating airway responses.
- The study suggests that Trim31 helps control the activation of the NLRP3 inflammasome, and its deficiency could worsen asthma symptoms, indicating that targeting Trim31 might be a promising treatment strategy for asthma.
Article Abstract
Tripartite motif (Trim) 31 is important for numerous inflammatory diseases. However, whether Trim31 regulates airway inflammation in asthma remains undetermined. The present work explored the role of Trim31 in airway inflammation in asthmatic mice established by ovalbumin (OVA) stimulation. Trim31 expression was markedly downregulated in the lungs of asthmatic mice. Compared with wild-type (WT) mice, Trim31 mice showed more severe pathological changes accompanied by increased inflammatory cell infiltration after OVA induction. House dust mite (HDM) stimulation evoked airway epithelial cell injury and inflammation, which were exacerbated by Trim31 silencing or attenuated by Trim31 overexpression. Further examination revealed that Trim31 deficiency exacerbated the activation of the NLRP3 inflammasome in OVA-induced asthmatic mice and HDM-stimulated airway epithelial cells. The inhibition of NLRP3 markedly diminished the Trim31 silencing-mediated enhancement of HDM-induced injury and inflammation in airway epithelial cells. In conclusion, this work demonstrates that Trim31 acts as a crucial mediator of airway inflammation in asthma. Trim31 deficiency may contribute to the progression of asthma by increasing NLRP3 inflammasome activation, suggesting that Trim31 is a potential therapeutic target for asthma.
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| http://dx.doi.org/10.1016/j.intimp.2024.112591 | DOI Listing |
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