炎症性肠病杂志

Inflammatory bowel disease (IBD) is a digestive tract disorder manifesting mainly in two forms, namely Crohn’s disease (inflammation of digestive tract) and ulcerative colitits (inflammation of large intestine lining) .Genetic and environmental factors could potentially predispose towards IBD. From a smoking perspective, ulcerative colitis is frequently observed in ex-smokers of non-smokers whereas Crohn’s disease is frequently observed among smokers. Smoking was reported to have distinct effects in these two types of disorders, nevertheless elicitation of humoral and cellular immunity was observed to be common in both the types of IBDs. Smoking has been implicated in disease amelioration in case of UC. However, smoking has been associated with several adverse effects including cardiovascular disease and carcinogenesis which outweigh the beneficial aspects. The present review collates information on the role of smoking in UC based on latest research outcomes and elucidates the effect of nicotine (an active constituent in smoking) and associated mechanism of action in IBD condition.

Genetic and environmental factors are the cause of disorders like inflammatory bowel diseases (IBD). Ulcerative colitis (UC) is a type of IBD which is mostly seen in non-smokers or former smokers. In UC protective effect of smoking is seen due to nicotine presence. While in Crohn’s disease (CD) smoking show opposite effects hence, it is complex to know relationship between IBD’s. Humoral and cellular immunity changes are indulged in the relationship of both the IBD’s. Therapeutically, nicotine is used for many diseases like ulcerative colitis, Alzheimer's disease, Parkinson's disease, Tourette's syndrome, sleep apnea, and attention deficit disorder. In case of active UC nicotine is effective while in most cases this nicotine becomes harmful and causes side effects like nausea, headache, dermatitis etc. Smoking is linked to most hazardous effects like atherosclerosis, pulmonary hypertension, cardiovascular diseases, carcinogenic disorders which make patients to quit smoking. This sudden ceasing of smoking may potentially elevate symptoms. Correlating with the previous data here we will compare effect of smoking based on genetic susceptibility, twins, gender, and smokers and non- smokers. Data is highly contradictory while the involved mechanism in both the cases is still unknown. In this paper we have mainly focused on smoking role in Ulcerative colitis (UC) depending on many studies done in recent years and also the effect and mechanism of nicotine action on our body.

Recently, symptomatic improvements with food exclusion diet based on immunoglobulin G (IgG) antibodies have been reported in both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). But the mechanisms of these results have not been explained yet. The common point of these disorders is the important role of mast cells in their pathogenesis. Mast cells are widely present in intestinal mucosa and they are responsible for both intestinal health and disorder status. IgG-antigen immune complexes can stimulate mast cells by binding to their activating Fcγ receptors. Increased IgG-food antigen complexes due to increased food specific IgG antibodies can cause more mast cell activation. Elimination of these foods may help symptomatic improvement in patients with IBD and IBS by reducing the amount of immune complexes because of lack of the food antigen part of them.