Anti-inflammatory effects of nicotine in obesity and ulcerative colitis
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REVIEW
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Anti-inflammatory effects of nicotine in obesity and ulcerative colitis Shaheen E Lakhan1* and Annette Kirchgessner1,2
Abstract Cigarette smoke is a major risk factor for a number of diseases including lung cancer and respiratory infections. Paradoxically, it also contains nicotine, an anti-inflammatory alkaloid. There is increasing evidence that smokers have a lower incidence of some inflammatory diseases, including ulcerative colitis, and the protective effect involves the activation of a cholinergic anti-inflammatory pathway that requires the a7 nicotinic acetylcholine receptor (a7nAChR) on immune cells. Obesity is characterized by chronic low-grade inflammation, which contributes to insulin resistance. Nicotine significantly improves glucose homeostasis and insulin sensitivity in genetically obese and diet-induced obese mice, which is associated with suppressed adipose tissue inflammation. Inflammation that results in disruption of the epithelial barrier is a hallmark of inflammatory bowel disease, and nicotine is protective in ulcerative colitis. This article summarizes current evidence for the anti-inflammatory effects of nicotine in obesity and ulcerative colitis. Selective agonists for the a7nAChR could represent a promising pharmacological strategy for the treatment of inflammation in obesity and ulcerative colitis. Nevertheless, we should keep in mind that the anti-inflammatory effects of nicotine could be mediated via the expression of several nAChRs on a particular target cell. Keywords: α7-nicotinic acetylcholine receptor, ulcerative colitis, enteric nervous system, pro-inflammatory cytokines
Introduction The major addictive component of tobacco, nicotine, exerts anti-inflammatory effects in multiple cell types and has been shown to benefit various disorders in which an inflammation-related mechanism is implicated. Chronic low-grade inflammation is a key feature of obesity, which is characterized by the elevated production of pro-inflammatory cytokines by the adipose tissue itself [1-3]. Chronic and relapsing inflammation is at the core of inflammatory bowel disease (IBD), which is characterized by activation of the pro-inflammatory transcription factor nuclear factor-B (NF-B) [4] and increased expression of pro-inflammatory cytokines such as tumor necrosis (TNF)-a in immune cells in the mucosa of IBD patients [5,6]. Nicotine has been proven effective in reducing obesity-related inflammation and insulin resistance [7] and attenuating inflammation and improving gut function in patients with active colitis [8]. In fact, ulcerative colitis patients with a history of * Correspondence: [email protected] 1 Global Neuroscience Initiative Foundation, Los Angeles, CA, USA Full list of author information is available at the end of the article
smoking usually acquire their disease after they have stopped smoking [9-11]. Patients who smoke intermittently often experience an improvement in their colitis symptoms during the periods when they smoke [9,12]. Therefore the development of drugs d
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