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 α7 nicotinic acetylcholine receptor (α7nAChR) 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 α7nAChR 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.
Highlights
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 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 significantly suppressed tumor necrosis factor (TNF)-a-induced cytokine production in wild type, but not a7 nicotinic acetylcholine receptor (a7nAChR) -/- macrophages [7]. These findings suggest that nicotine and specific a7nAChR agonists may be beneficial in the prevention and treatment of obesity-induced inflammation and insulin resistance
Summary
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. Activation of the cholinergic anti-inflammatory pathway by low-dose nicotine significantly suppressed inflammation in adipose tissue, an important site in mediating obesityinduced inflammation in genetically obese (db/db) and diet-induced obese (DIO) mice This was associated with a significant improvement in glucose homeostasis and insulin sensitivity without changes in body weight. Macrophages isolated from mice deficient in a7nAChR had elevated pro-inflammatory cytokine production in response to free fatty acids and TNF-a, known agents causing inflammation and insulin resistance. Nicotine significantly suppressed TNF-a-induced cytokine production in wild type, but not a7nAChR -/- macrophages [7] Overall, these findings suggest that nicotine and specific a7nAChR agonists may be beneficial in the prevention and treatment of obesity-induced inflammation and insulin resistance.
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