Colitis-Aid.com

Scientists search for drug candidates in some very unlikely places. Not only do they churn out synthetic compounds in industrial-scale laboratories, but they also scour coral reefs and scrape tree bark in the hope of stumbling upon an unsuspecting molecule that just might turn into next year’s big block buster. But one region that scientists have not been searching is their guts. Literally.

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In rats with experimental colitis, the marked increase in bacterial translocation in postcolitis rats has been reversed by melatonin administration. This is due to melatonin’s anti-inflammatory and anti-apoptotic effects.

Using an elegant study design, including experimental colitis model, this research was performed by doctors from the Departments of General Surgery, Microbiology, Pathology and Biochemistry of the Faculty of Medicine at the University of Erciyes, Kayseri, Turkey.

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The body’s first line of defence against pathogenic bacteria that we ingest may not be the immune system but rather the cells that line the intestine. This surprising conclusion is just one facet of a study by Dr. Maya Saleh, a researcher at the Research institute of the McGill University Health Centre that will be published in the journal Cell Host & Microbe on March 12.This, and the various mechanisms revealed by this discovery, could lead to important therapeutic innovations, particularly in the treatment of diarrheal diseases and inflammatory bowel diseases such as Crohn’s disease.

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Individuals with the inflammatory bowel disease ulcerative colitis are at increased risk of developing colon cancer. New data generated by Naofumi Mukaida and colleagues at Kanazawa University, Japan, identified a central role for the soluble factor TNF-alpha in the development of colon cancer in mice in which inflammation of the bowel was induced by administration of azoxymethane (AOM) followed by repeated dextran sulfate sodium (DSS) ingestion. Expression of TNF-alpha was increased in the colon of normal mice treated with AOM and DSS and this was followed by the development of tumors in the colon. Mice lacking one of the receptors for TNF-alpha and mice treated with an antagonist of TNF-alpha were markedly protected from the effects of treatment with AOM and DSS, developing less inflammation of the colon and fewer tumors in the colon. As suggested by the authors, and by Ezra Burstein and Eric R. Fearon in an accompanying commentary, these data provide clear rationale for the idea that drugs antagonizing TNF-alpha (such as those used to treat individuals with rheumatoid arthritis) might be useful in reducing the risk of colon cancer in individuals with ulcerative colitis.

The gastrointestinal (GI) tract is colonized by bacteria immediately after birth; Escherichia coli, Streptococci and Clostridi are the first bacteria harboured by the colon, followed by anaerobic Enterococci, Lattobacilli and Bacteroidi. These commensal bacteria inhabiting the human intestine (i.e., intestinal microflora) participate in the development and maintenance of gut sensory and motor functions, including the promotion of intestinal propulsive activity; on the other hand, intestinal motility represents one of the major control systems of gut microflora, though the sweeping of excessive bacteria from the lumen. There is emerging evidence indicating that changes in this bi-directional interplay contribute to the pathogenesis of gut diseases, such as small intestinal bacterial overgrowth (SIBO). 

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Nearly three out of four patients with ulcerative colitis (UC) consider feeling unwell to be a normal part of life, while gastroenterologists estimate this to be true for only 37 percent of their UC patients, according to results from a nationwide series of surveys presented today at the 2007 Crohn’s & Colitis Foundation’s 6th Annual Advances in the Inflammatory Bowel Diseases conference.  

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Researchers have found a potential new and improved avenue for treating defective bile acid absorption, a primary contributor to chronic diarrhea.

Liver-produced bile acids are intestinal detergents that break apart fats for easier absorption. Normally, most of the bile acids also reabsorb, but during certain conditions (e.g. infection or short bowel syndrome) excess bile acids enter the colon and impair water absorption, leading to diarrhea.

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While chronic inflammation is a known risk factor for atherosclerosis (hardening of the arteries) and heart disease, researchers have now shown that the sporadic but recurrent inflammation caused by Crohn’s disease also poses serious cardiovascular risk.

Sander van Leuven and his colleagues imaged 60 Crohn’s patients and 122 healthy controls for signs of arterial hardening; they found that the thickness of the carotid artery, a common marker for plaque buildup, was increased in Crohn’s disease.

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