Cigarette Smoke Extract Induces Inflammation by RELMβ via NF-κB/p65 Signaling in Chronic Obstructive Pulmonary...

This study aims to investigate the regulatory effects of cigarette smoke extract (CSE) on resistin-like molecule β (RELMβ) in chronic obstructive pulmonary disease (COPD) and to elucidate the mechanisms by which RELMβ modulates inflammatory factors.

The expression of RELMβ in 16HBE cells after CSE exposure was detected. The activation and nuclear translocation of NF-κB/p65, degradation of IκBα protein, and the expression of inflammatory factors were assessed in 16HBE cells with RELMβ overexpression or exogenous human recombinant RELMβ protein stimulation.

CSE exposure promoted mRNA and protein expression of RELMβ in 16HBE cells. Both stable overexpression of RELMβ and exogenous recombinant RELMβ protein stimulation enhanced secretion of IL-1β, IL-8, IL-6, and TNF-α, upregulated mRNA expression of IL-1β and IL-8, increased phosphorylation of p-IKKα/β, p-IκBα, and p-NF-κB/p65, promoted nuclear translocation of NF-κB/p65, and accelerated the degradation of IκBα in a dose-dependent and time-dependent manner. Inhibition of the NF-κB signaling pathway using pyrrolidine dithiocarbamate and Bay 11-7082 blocked the promotion effect of CSE and RELMβ on expression of p-NF-κB/p65, IL-1β, and IL-8.

CSE induces inflammation via RELMβ through NF-κB/p65 signaling pathway in COPD. This study provides new insights into the involvement of CSE in the progression of COPD from the perspective of RELMβ.