The Role of Human Defensins in Gastrointestinal Diseases

Jost Langhorst; Kyung-Eun Choi


Expert Rev Clin Immunol. 2011;7(6):779-787. 

In This Article

Special Role for Defensins in IBD

Inflammatory bowel disease subsumes CD and UC as main types of chronic inflammation of the intestine, distinguished on the basis of their clinical features and histopathology. Since the precise mechanisms of the pathogenesis of both diseases remain unclear therapeutic approaches commonly focus on symptom reduction.

The inflamed tissue seen in patients with UC is typically restricted to the colon, while that of CD occurs in the whole GI tract, most commonly in the small intestinal ileum and in the colon.[4] The first occurrence of CD often starts after a bacterial infection[43] and there is high evidence that its development is associated with high hygiene standards as well as a frequent use of antibiotics during childhood,[44] two factors that have also been discussed in the pathogenesis of other IBD.[45] Intestinal microbes in the form of commensal microbiota may trigger the disease in genetically susceptible individuals.[46] High concentrations of adherent and sometimes invading luminal bacteria were shown in colonic biopsies in both inflamed and noninflamed mucosa from IBD patients in contrast to those of healthy individuals.[47]

In line with the assumption that reduced concentrations of AMPs may compromise host defence and predispose to IBD,[3] cumulative evidence shows how different HD defects may explain the specific anatomic patterns of affected areas; the constitutively expressed HBD-1 is reduced in CD and UC patients, while the inducible HBD-2 and -3 levels correlate with inflammation in IBD,[12] with HBD-2 being distinctively expressed in the case of UC and CD.[12] Furthermore, previous studies describe defensin deficiency in the colon against different bacteria including Bacteroides vulgatus, E. coli and Enterococcus faecalis for CD compared with UC.[48] A deficient defensin expression – that is, an attenuated induction of the inducible β-catenins – may therefore underlie the chronic inflammation of CD. Remarkably, probiotic bacteria also enhance the level of HBD-2 in intestinal epithelial cells.[28]


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