Cigarette smoking and gastrointestinal diseases: The causal relationship and underlying molecular mechanisms (Review)

• Published in: International journal of molecular medicine Vol. 34; no. 2; pp. 372 - 380
• Main Authors: LI, L.F, CHAN, R.L.Y, LU, L, SHEN, J, ZHANG, L, WU, W.K.K, WANG, L, HU, T, LI, M.X, CHO, C.H
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01-08-2014; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Angiogenesis; cancer; Carcinogenesis - drug effects; Cell Death - drug effects; Cell growth; Chemokines; Cigarettes; Colorectal cancer; Disease; Disease susceptibility; Gastric Mucosa - drug effects; Gastric Mucosa - pathology; Gastrointestinal diseases; Gastrointestinal Diseases - etiology; Gastrointestinal Diseases - pathology; Genetic aspects; Health aspects; Health risk assessment; Humans; Immune system; Infections; Inflammation; Inflammatory bowel disease; Inflammatory diseases; Lung cancer; Neutrophils; Polyamines; Risk Factors; Smoking; Smoking - adverse effects; Stomach Neoplasms - etiology; Stomach Neoplasms - pathology; Studies; Tobacco; Tumorigenesis; Ulcers
• ISSN: 1107-3756; 1791-244X
• DOI: 10.3892/ijmm.2014.1786

Cigarette smoking is an important risk factor for gastrointestinal (GI) disorders, including peptic ulcers, inflammatory bowel diseases, such as Crohn's disease and cancer. In this review, the relationship between smoking and GI disorders and the underlying mechanisms are discussed. It has been demonstrated that cigarette smoking is positively associated with the pathogenesis of peptic ulcers and the delay of ulcer healing. Mechanistic studies have shown that cigarette smoke and its active ingredients can cause mucosal cell death, inhibit cell renewal, decrease blood flow in the GI mucosa and interfere with the mucosal immune system. Cigarette smoking is also an independent risk factor for various types of cancer of the GI tract. In this review, we also summarize the mechanisms through which cigarette smoking induces tumorigenesis and promotes the development of cancer in various sections of the GI tract. These mechanisms include the activation of nicotinic acetylcholine receptors, the formation of DNA adducts, the stimulation of tumor angiogenesis and the modulation of immune responses in the GI mucosa. A full understanding of these pathogenic mechanisms may help us to develop more effective therapies for GI disorders in the future.