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7, 8, 16 Nicotine, an anti-inflammatory alkaloid, activates the nicotine receptor 7 (7-nAChR) in immune cells, suppresses the production of pro-inflammatory cytokines, and facilitates the production of anti-inflammatory cytokines.17, 18, 19 The nAChR is also present in endothelial cells, where nicotine suppresses the molecules needed for immune cell migration in IBD.20 After smoking cessation, the activity of nAChR fluctuates, which may dysregulate the immune system, making ex-smokers more prone to the development of UC.21 Nicotine affects the number of nAChRs differently in adolescents compared to adults, contributing to the increase of UC risk in young ex-smokers.22 Moreover, cigarette smoke contains nicotine and other substances, such as carbon monoxide, nitrogen oxides, and cadmium, that influence the immune system.23 Sex-dependent differences in UC according to smoking experience have been previously reported

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