Cigarette Smoking Contributes to Th1/Th2 Cell Dysfunction via the Cytokine Milieu in Chronic Obstructive Pulmonary Disease

• DOI: 10.2147/copd.s426215
• Publication Date: 2023-09-12T04:10:36Z
• Authors: Gang Chen; Qing Mu; Zhao-Ji Meng
• Keywords: nicotinic acetylcholine receptors ;nachrs; RC705-779; cigarette smoke; Interleukin-18; copd; t helper 1 ;th1 cells; International Journal of Chronic Obstructive Pulmonary Disease; 3. Good health; chronic obstructive pulmonary disease; Cigarette Smoking; th2; Diseases of the respiratory system; Pulmonary Disease, Chronic Obstructive; Th2 Cells; Humans; Cytokines; Original Research

Background: Dysregulation and pyroptosis of T-helper (Th) cells inflammatory cytokines have been implicated in the pathogenesis chronic obstructive pulmonary disease (COPD). However, immune response mechanisms as a consequence tobacco smoke exposure are not fully understood. We hypothesized that cigarette smoke-induced inflammation could be modulated through cytokine milieu T-cell nicotinic acetylcholine receptors (nAChRs). Methods: The proportions peripheral blood Th1 Th2 from patients with COPD, smokers without airway obstruction healthy nonsmokers were analyzed using flow cytometry. levels plasma proinflammatory their potential association function also measured. influence extract (CSE) on conditioned differentiation T helper cell subsets was further examined vitro. Results: Significantly higher IFN-γ IL-18 but lower found COPD. increased negatively correlated (FEV1% predicted value). Pyroptosis participates COPD development probably activation NLRP3 inflammasome upon to CSE. CSE does directly induce cells; however, under medium, promotes α 7 nAChR modification, while it substantially interfere differentiation. Conclusion: differences play key role effects Keywords: disease, smoke, 1, cells, Th2, receptors, nAChRs