Abstract
Cigarette smoke (CS) has adverse effects in patients with Crohn’s disease (CD), an inflammatory bowel disease (IBD) that has been associated with microbial infection, immuno-dysregulation, and mucosal dysfunction. However, CS seems to provide relief and protection to patients with another IBD known as ulcerative colitis (UC). These two subsets are featured as M1- and M2-mediated responses, respectively. Nicotine is the most active, addictive, and studied ingredient in CS. The mechanism of how nicotine and/or other CS ingredients induce pro-inflammatory or anti-inflammatory phenotypes in IBD patients remains under investigation. Our most recent in vitro nicotine study provided significant insights toward understanding the contradictory effects of nicotine on IBD patients, and it elucidated the mechanistic role of α7nAChR in modulation of macrophages in tobacco smokers. Shifting the beneficial effect of nicotine to a harmful outcome in CD patients was linked to a nicotine-microbe interaction that supports a microbial etiology in CD pathogenesis. Among the most debated pathogens in CD etiology is Mycobacterium avium subspecies paratuberculosis (MAP). Other studies associated nicotine with upregulation of miR-124 expression in macrophages, which led to anti-inflammatory response. This review discusses published work on the role of nicotine in modulation of the innate immune response and subsequent signaling in macrophages in IBD subsets.
Highlights
Inflammatory bowel disease (IBD) is a chronic condition that involves severe inflammation in the lining of the digestive tract [1]
Variants of human leukocyte antigen (HLA) haplotypes as HLA class II allele DRBI*0103 have been strongly associated with ulcerative colitis (UC), whereas nucleotide-binding oligomerization domain-containing protein 2 (NOD2) polymorphisms have been linked to Crohn’s disease (CD) [5]
Other factors have been associated with CD pathogenesis, and not UC, such as environmental triggers including diet, UV light exposure, vitamin D deficiency, infection, and tobacco smoking
Summary
Inflammatory bowel disease (IBD) is a chronic condition that involves severe inflammation in the lining of the digestive tract [1]. Smoking tobacco not just always exacerbates symptoms in CD patients, it causes higher risk of relapse than non-smokers with CD [10,11] To understand this dogma in IBD subsets, our research team has been investigating the effects of cigarette smoke and nicotine on the cellular and molecular changes in CD- and UC-like macrophages. AlQasrawi et al reported recently that they were able to mimic macrophages similar to those in CD and UC patients with history of prior or active cigarette smoking and studied cellular response in the presence and absence of active bacterial infection [12] Among the findings, they elucidated how nicotine in UC active smokers activates the cholinergic anti-inflammatory pathway through α7-nicotinic acetylcholine receptor (α7nAChRs). This study will focus more on interplay between infection and smoking and their effects on IBD patients
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