3.8 Review

Antimicrobial Proteins in Intestine and Inflammatory Bowel Diseases

Journal

INTESTINAL RESEARCH
Volume 12, Issue 1, Pages 20-33

Publisher

KOREAN ASSOC STUDY INTESTINAL DISEASES
DOI: 10.5217/ir.2014.12.1.20

Keywords

Antimicrobial protein; Antimicrobial peptide; Colitis; Inflammatory bowel diseases

Funding

  1. Basic Science Research Program through the National Research Foundation of Korea - Ministry of Education, Science, and Technology (MEST) [NRF-2013R1A1A2A10004404]
  2. MRC program through the National Research Foundation of Korea - Ministry of Education, Science, and Technology (MEST) [NRF-2008-0062287]

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Mucosal surface of the intestinal tract is continuously exposed to a large number of microorganisms. To manage the substantial microbial exposure, epithelial surfaces produce a diverse arsenal of antimicrobial proteins (AMPs) that directly kill or inhibit the growth of microorganisms. Thus, AMPs are important components of innate immunity in the gut mucosa. They are frequently expressed in response to colonic inflammation and infection. Expression of many AMPs, including human beta-defensin 2-4 and cathelicidin, is induced in response to invasion of pathogens or enteric microbiota into the mucosal barrier. In contrast, some AMPs, including human alpha-defensin 5-6 and human beta-defensin 1, are constitutively expressed without microbial contact or invasion. In addition, specific AMPs are reported to be associated with inflammatory bowel disease (IBD) due to altered expression of AMPs or development of autoantibodies against AMPs. The advanced knowledge for AMPs expression in IBD can lead to its potential use as biomarkers for disease activity. Although the administration of exogenous AMPs as therapeutic strategies against IBD is still at an early stage of development, augmented induction of endogenous AMPs may be another interesting future research direction for the protective and therapeutic purposes. This review discusses new advances in our understanding of how intestinal AMPs protect against pathogens and contribute to pathophysiology of IBD.

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