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Smoking and IBD
The relationship between smoking cigarettes and inflammatory bowel disease (IBD) is now firmly established but remains a source of confusion among both patients and doctors. The literature strongly supports the fact that smoking cigarettes is associated with Crohn's disease (CD) and that nonsmoking is associated with ulcerative colitis (UC). CD patients who are smokers suffer from severe episodes of the disease, indicated by a flare-up of inflammation and acute symptoms. As in UC patients and healthy controls, these symptoms are limited in those CD patients who are nonsmokers. The chronic, transmural, and debilitating inflammatory disorder of the gastrointestinal tract in CD patients has been associated with Mycobacterium avium subsp. paratuberculosis (MAP), a fastidious, acid-fast bacillus responsible for similar IBD in cattle. Nicotine is considered to be the most pharmacologically active and addictive substance among the many compounds present in tobacco products. Why does smoking increase the risk of developing CD and the risk of disease recurrence after an operation for CD? Why does smoking decrease the risk of developing UC? We were astonished to see the enormous amount of data that associates smoking cigarettes with CD that addressed the negative effect on the clinical course of it in these patients. However, the current literature provides limited explanations regarding the mechanism of the effect of smoking and IBD. We recently evaluated the effect of nicotine, using the Bactec system, on several microorganisms, including MAP, the suspected etiological agent in some CD cases. The minimum inhibitory concentration (MIC) was at least 50 times lower than the nicotine level in saliva of smokers who smoke 10 cigarettes per day. The data confirmed that nicotine's effect is bactericidal, leading to the destruction and degradation of MAP and maybe other microorganisms. We speculate that the inconsistent, high level of nicotine in CD patients who smoke may affect the MAP or other microorganism residing in ulcerated mucosal cells. Consequently, numerous antigens or groups of antigens (some of which have strong cross- reactivity with intestinal proteins) may be released, causing a strong inflammatory immune response. This may lead to an acute CD presence in tobacco users versus nonsmoking CD patients or other controls regardless of their tobacco habits. Alternatively, nicotine's inhibitory effect on normal intestinal flora such as Escherichia coli and Staphylococcus spp. could enable opportunistic pathogens to proliferate and serve as foci for subsequent infections. Clearly, the effect of nicotine on pathogens and normal flora needs to be elucidated. The outcome would provide significant data toward either a beneficiary use of nicotine to treat infectious diseases or nicotine's role in causing subsequent infections and complications in mucosal conditions.
Saleh A. Naser
George Ghobrial
University of Central Florida, Orlando
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