Inflammatory bowel disease pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Pathophysiology[edit | edit source]

A recent hypothesis posits that some IBD cases are caused by an overactive immune system attacking various tissues of the digestive tract because of the lack of traditional targets such as parasites and worms. The number of people being diagnosed with IBD has increased as the number of infections by parasites, such as roundworm, hookworm and human whipworms, has fallen, and the condition is still rare in countries where parasitic infections are common. This is similar to the hygiene hypothesis applied to allergies.

Initial reports (Summers et al 2003) suggest that helminthic therapy may not only prevent but even cure (or control) IBD: a drink with roughly 2,500 ova of the Trichuris suis helminth taken twice monthly decreased symptoms markedly in many patients. It is even speculated that an effective immunization procedure could be developed—by ingesting the cocktail at an early age.

Prebiotics and probiotics are showing increasing promise as treatments for IBD (Furrie, 2005) and in some studies have proven to be as effective as prescription drugs (Kruis, 2004).

More recently, research (Hue et al 2006) has shown that IL-23 is overexpressed in tissues taken from mouse models of IBD. The group showed that knocking out IL-23 (heterodimer of IL-12p40 and IL-23p19) severely reduced inflammation of the bowel, both in terms of cells and proinflammatory cytokine production. Also, they found that a novel group of CD4⁺ T lymphocytes, Th17 T cells, are highly upregulated in bowels of diseased mice. Taken together, the group shows that IL-23 but not IL-12 (IL-12p40 and IL-12p35; share a subunit) drives innate and T cell mediated intestinal inflammation.

References[edit | edit source]