Time Relationships between Cessation of Smoking and Onset of Ulcerative Colitis

Motley, Richard; Rhodes, J.; Ford, GA; Wilkinson, S. P.; Chesner, I. M.; Asquith, P.; Hellier, M. D.; Mayberry, J. F.

doi:10.1159/000199478

Cited by 110 publications

(49 citation statements)

References 5 publications

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“…Current smoking decreased the risk for UC (OR: 0.58; 95% CI: 0.45-0.75), while former smoking was associated with an increased risk (OR: 1.79; 95% CI: 1.37-2.34). Interestingly, in patients who stopped smoking, UC developed in 52% of patients, in the first three years after cessation, as reported by Motley et al [12] in concordance with other studies [13] . In contrast, active smoking in early childhood was associated with a gradually increased risk for developing UC (OR for smoking start < 10 years: 7.02 and < 15 years: 3.46) [14] .…”

Section: Risk For Developing Ulcerative Colitissupporting

confidence: 87%

“…In intermittent smokers, many patients note symptom exacerbation when they stop smoking, followed by symptom relief when they smoke again [12] . In contrast, almost half of the intermittent smokers thought that their colitis symptoms improved while smoking at least 20 cigarettes per day [32] .…”

Section: Effect Of Smoking and Its Cessation On Clinical Course And Ementioning

confidence: 99%

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Smoking in inflammatory bowel diseases: Good, bad or ugly?

Lakatos¹,

Szamosi²,

Lakatos³

2007

WJG

133

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Smoking is an important environmental factor in inflammatory bowel disease (IBD), having different effects in ulcerative colitis (UC) and Crohn's disease (CD). A recent meta-analysis partially confirmed previous findings that smoking was found to be p r o t e c t i v e a g a i n s t u l c e r a t i v e c o l i t i s a n d , a f t e r onset of the disease, might improve its course, d e c r e a s i n g t h e n e e d f o r c o l e c t o m y . H o w e v e r , smoking increases the risk of developing Crohn's disease and worsens its course, increasing the need for steroids, immunosuppressants and re-operations. Smoking cessation aggravates ulcerative colitis and improves Crohn's disease. Data are however, largely conflictive as well as the potential mechanisms involved in this dual relationship are still unknown. In this review article, the authors review the role of smoking in inflammatory bowel diseases.

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Section: Risk For Developing Ulcerative Colitissupporting

confidence: 87%

Section: Effect Of Smoking and Its Cessation On Clinical Course And Ementioning

confidence: 99%

Smoking in inflammatory bowel diseases: Good, bad or ugly?

Lakatos¹,

Szamosi²,

Lakatos³

2007

WJG

133

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“…Therefore, the nicotine transport system is suggested to be independent of the tertiary amine transport system. There has been overwhelming epidemiological evidence that smoking protects against ulcerative colitis (Motley et al, 1987;Odes et al, 2001). The mechanisms through which nicotine may affect the course of colitis may be relevant to the pathogenesis of this disease.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, ulcerative colitis usually occurs in nonsmokers, and especially among former smokers with ulcerative colitis, the disease typically begins after smoking cessation (Motley et al, 1987;Odes et al, 2001). Although the precise mechanisms of this protective role of tobacco smoke are not clear, nicotine, known to be a major psychoactive compound of tobacco smoke, is suggested to play a major role in it.…”

mentioning

confidence: 99%

Transport Mechanisms of Nicotine across the Human Intestinal Epithelial Cell Line Caco-2

Fukada¹,

Saya²,

Inui³

2002

J Pharmacol Exp Ther

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Ulcerative colitis is a disease more commonly seen in nonsmokers. Because nicotine was postulated to be a beneficial component of tobacco smoke for ulcerative colitis, various formulations of nicotine have been developed to improve the local bioavailability within the gastrointestinal tissue. In the present study, to characterize the disposition of nicotine in the intestines, we investigated intestinal nicotine transport using Caco-2 cells. Nicotine was predominantly transported across Caco-2 cell monolayers in a unidirectional mode, corresponding to intestinal secretion, by pH-dependent specific transport systems. The specific uptake systems appear to be distinct from organic cation transporters and the transport system for tertiary amines, in terms of its substrate specificity and the pattern of the interaction. These transport systems could play a role in the intestinal accumulation of nicotine from plasma and could also be responsible for the topical delivery of nicotine for ulcerative colitis therapy. These findings could provide useful information for the design of effective nicotine delivery.

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“…[73][74][75] In addition, many ulcerative colitis patients noted disease exacerbation upon cessation of smoking, whereas symptoms relief is reported when smoking is resumed. 76 Although there is no clear explanation for this difference, a recent report using two models of murine colitis mimicking Th1 or Th2 type of inflammation has shown that the divergent effect of nicotine may be explained by the upregulation of the α7nAChR by a Th2 inflammatory response (ulcerative colitis) but not by a typical Th1/Th17 inflammatory response. 77 Assuming that the therapeutic response of nicotine (or smoking) is mediated by α7nAChR, these findings may explain the differential effect of smoking in Crohn's versus ulcerative colitis patients.…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

The vagal innervation of the gut and immune homeostasis

Matteoli

Gomez‐Pinilla

Giovangiulio

et al. 2015

Autonomic Neuroscience

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The central nervous system interacts dynamically with the immune system to modulate inflammation through humoral and neural pathways. Recently, in animal models of sepsis, the vagus nerve (VN) has been proposed to play a crucial role in the regulation of the immune response, also referred to as the cholinergic anti-inflammatory pathway. The VN, through release of acetylcholine, dampens immune cell activation by interacting with α-7 nicotinic acetylcholine receptors. Recent evidence suggests that the vagal innervation of the gastrointestinal tract also plays a major role controlling intestinal immune activation. Indeed, VN electrical stimulation potently reduces intestinal inflammation restoring intestinal homeostasis, whereas vagotomy has the reverse effect. In this review, we will discuss the current understanding concerning the mechanisms and effects involved in the cholinergic anti-inflammatory pathway in the gastrointestinal tract. Deeper investigation on this counter-regulatory neuroimmune mechanism will provide new insights in the cross-talk between the nervous and immune system leading to the identification of new therapeutic targets to treat intestinal immune disease.

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Time Relationships between Cessation of Smoking and Onset of Ulcerative Colitis

Cited by 110 publications

References 5 publications

Smoking in inflammatory bowel diseases: Good, bad or ugly?

Smoking in inflammatory bowel diseases: Good, bad or ugly?

Transport Mechanisms of Nicotine across the Human Intestinal Epithelial Cell Line Caco-2

The vagal innervation of the gut and immune homeostasis

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