The Inflammatory Response Induced by RELMβ Upregulates IL-8 and IL-1β Expression in Bronchial Epithelial Cells in COPD

Purpose: Chronic obstructive pulmonary disease (COPD) is associated with a complex inflammatory regulatory network. Resistin-like molecule beta (RELM beta) is highly expressed in the lungs of COPD patients. We aimed to investigate the proinflammatory effect of RELM beta on airway epithelial cells in COPD. Methods: First, a GEO dataset was used to analyze the expression of the RELM beta gene in the COPD and control groups as well as the protein levels of RELM beta in the sera of outpatients with COPD and normal control subjects in our hospital. We also stimulated 16HBE bronchial epithelial cells with recombinant RELM beta protein and analyzed the expression of IL-8 and IL-1 beta. We upregulated and downregulated the gene expression of RELM beta in 16HBE cells and analyzed the expression of the inflammatory cytokines IL-8 and IL-1 beta. In addition, we also examined the mechanism by which the p38 MAPK signaling pathway contributed to the regulation of IL-8 and IL-1 beta expression by RELM beta. Results: RELM beta expression was increased in COPD tissues in different data sets and in the serum of COPD patients in our hospital. IL-8 and IL-1 beta expression was also increased in COPD tissues with high RELM beta gene expression in different data sets. The RELM beta gene was mainly related to inflammatory factors and inflammatory signaling pathways in the PPI regulatory network. Experiments at the cellular level showed that RELM beta promoted the expression of the inflammatory cytokines IL-8 and IL-1 beta, and this regulation was mediated by the p38 MAPK signaling pathway. Conclusion: RELM beta can promote the expression of the inflammatory cytokines IL-8 and IL-1 beta in bronchial epithelial cells of patients with COPD and exert inflammatory effects. RELM beta may be a potential target for the treatment of COPD.

Automated summary

The research found that RELM beta can promote the expression of inflammatory cytokines IL-8 and IL-1 beta in airway epithelial cells of COPD patients, and this effect is mediated by the p38 MAPK signaling pathway. Therefore, RELM beta may be a potential target for the treatment of COPD.