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- W4310343135 abstract "Abstract Background: Epithelial barrier is important for asthma development by shaping immune responses. Airway expressing-IL-1 receptor-associated kinase (IRAK)-M of Toll-like receptor pathway is involved in immunoregulation of airway inflammation through influencing activities of macrophages and dendritic cells or T cell differentiation. IRAK-M is highly inducible in lung epithelial cells. Whether IRAK-M has effect on cellular immunity in airway epithelial cells in response to external stimulation remains unclear. Methods: We modeled cellular inflammation induced by IL-1β, TNF-α, IL-33, and house dust mite (HDM) in A549 cells. Cytokine production and pathway activation were used to reflect the effects of IRAK-M siRNA knockdown on epithelial immunity. The findings in A549 were validated in BEAS-2B cells. Genotyping an asthma-susceptible IRAK-M SNP rs1624395 and measurement of serum CXCL-10 levels were performed in asthma patients. Results: IRAK-M expression was significantly induced in A549 and BEAS-2B cells after stimulation. IRAK-M knockdown increased the production of cytokines and chemokines, including IL-6, IL-8, CXCL10, and CXCL11, at both mRNA and protein levels. Lung epithelial cells showed excessive activation of JNK and p38 MAPK pathways by IRAK-M silencing after stimulation. While antagonizing JNK or p38 MAPK inhibited increased secretion of CXCL10 mediated by IRAK-M silencing in cells. Asthma patients carrying G/G genotypes had significantly higher levels of serum CXCL-10 than those carrying homozygote A/A. Conclusion: Our findings suggested that the immunoregulatory effect of IRAK-M on lung epithelial inflammation, with a particular impact on CXCL10 production via JNK and p38 MAPK pathways. IRAK-M modulation might indicate a new insight into asthma pathogenesis from disease origin." @default.
- W4310343135 created "2022-12-09" @default.
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- W4310343135 date "2022-11-29" @default.
- W4310343135 modified "2023-10-18" @default.
- W4310343135 title "Title：IRAK-M has effects in regulation of lung epithelial inflammation through JNK and p38 MAPK pathways" @default.
- W4310343135 doi "https://doi.org/10.21203/rs.3.rs-2290842/v1" @default.
- W4310343135 hasPublicationYear "2022" @default.
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