CS can stimulate alveolar macrophages to release pro-inflammatory cytokines (e.g., IL-1β, TNF) through autocrine and paracrine mechanisms, triggering more severe inflammatory responses by inducing the release of pro-inflammatory and pro-fibrotic cytokines (e.g., IL-17, TGF-β, IFN-γ, VEGF, NLRP3) from recruited neutrophils and T lymphocytes, further exacerbating pulmonary inflammation and fibrosis (39–42). The gene discussed is IL17A; the disease is inflammatory response.