The Mechanisms of Resistin-Like Molecule-ß-Mediated Airway Inflammation in Chronic Obstructive Pulmonary Disease via Autophagy.

Background: The role of irreversible airway inflammatory damage in chronic obstructive pulmonary disease (COPD) progression is evident. Autophagy is an essential process in the cellular material metabolic cycle, and a family of resistant vegetative molecules may be involved in the COPD autophagic process. In this study, we investigated the mechanism of resistin-like molecule ß (RELMß) in COPD smoking-induced autophagy. Methods: Firstly, the expression differences of RELMß and autophagy markers between COPD and control groups were analyzed in the Gene Expression Omnibus (GEO) datasets and clinical specimens. Secondly, in vitro and in vivo experiments were conducted using immunoblotting, immunofluorescence, immunohistochemistry, and other methods to investigate the mechanism by which RELMß promotes airway inflammation through autophagy in a cigarette smoke extract-induced 16HBE cell inflammation model and a cigarette smoke-induced COPD-like mouse model. In addition, immunoprecipitation was used to analyze the binding of RELMß to the membrane protein TLR4. Results: The expression of RELMß and autophagy genes p62 and LC3B in lung tissue of COPD patients was significantly increased. RELMß can mediate the activation of autophagy in 16HBE cells, and through autophagy, it increases the expression of inflammatory cytokines in a cigarette smoke extract-induced 16HBE cell inflammation model. RELMß promotes cigarette smoke-induced COPD-like mouse airway inflammation through autophagy, and RELMß can mediate signal transduction through the cell membrane receptor TLR4. Conclusion: The RELMß binds to TLR4 to encourage signal transduction and that RELMß can promote inflammation in smoky COPD lungs through autophagy.