Although the etiology of inflammatory bowel disease (IBD) is not clearly understood, a combination of genetic, immunological, microbial, and environmental factors is thought to affect the disease.1,2 Currently, smoking appears to be the most closely related environmental factor for IBD. However, the effect of smoking is different for ulcerative colitis (UC) and Crohn’s disease (CD). Smoking increases the risk of CD by 2-fold and is correlated with a worse trajectory, increasing the risk of surgery. After remission, smokers have a higher risk of recurrence compared with nonsmokers.3,4 On the contrary, smoking reduces the risk of UC and patients who are currently smoking have a milder disease course while there is also a higher frequency of flares after quitting smoking. The mechanism of how smoking causes these effects on IBD remains unclear. In one study, blood mononuclear cells of smokers with CD and UC exhibited different chemokine and cytokine responses to oxidative stress, explaining its dual role in the pathogenesis of these two diseases.5
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Park et al. (2017) studied this question.
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