The effect of smoking on intestinal inflammation: what can be learned from animal models?

J Crohns Colitis. 2012 Feb;6(1):1-12. doi: 10.1016/j.crohns.2011.09.006. Epub 2011 Oct 12.

Abstract

Epidemiological evidence demonstrates that smoking is the most important environmental risk factor in Crohn's disease while it positively interferes with the disease course of ulcerative colitis. However, the underlying mechanisms through which smoking exerts this divergent effect and affects pathogenesis of inflammatory bowel disease are largely unknown. Animal smoke models are good models to investigate the impact of cigarette smoke on intestinal physiology and inflammation. They enable one to explore the interaction of smoke components and the gut on cellular and molecular level, clarifying how smoking interferes with normal gut function and with disease course in inflammatory conditions. This review describes the currently used animal models for studying the impact of cigarette smoke on the intestinal tract. We first discuss the different methods for simulation of smoking. Furthermore, we focus on the effect of smoke exposure on normal gut physiology and immunology, on experimental (entero)colitis, and on inflammation-induced neoplasia. Based on this current knowledge, a hypothesis is formulated about the mechanisms through which cigarette smoke interferes with the gut in normal and pathological conditions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / physiopathology*
  • Intestinal Neoplasms / physiopathology
  • Intestines / drug effects*
  • Intestines / pathology
  • Intestines / physiopathology
  • Models, Animal*
  • Nicotiana / adverse effects*
  • Nicotine / adverse effects*
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Risk Factors
  • Smoking / adverse effects*

Substances

  • Nicotine