Probiotics and inflammatory bowel disease

John H. Kwon, Richard J. Farrell

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations

Abstract

Inflammatory bowel disease (IBD) is characterised by a chronic dysregulation of the inflammatory response in the gastrointestinal tract. While the pathogenesis is unclear, studies have demonstrated that the gastrointestinal tracts of patients with IBD are populated with increased levels of adherent and pathogenic bacteria. This evidence, combined with growing data accumulated from genetic studies as well as animal models of IBD, indicates that an aberrant response to altered enteric flora plays a significant role in the disease process. Current therapies for IBD have been directed towards the development of anti-inflammatory agents and immunomodulators to attenuate the inflammatory response in the gastrointestinal tract. Antibiotics are also partially effective in the treatment of IBD, presumably by altering the bowel flora. However, it is clear from clinical trials that immunomodulators and antibiotics are not effective in a large proportion of patients with IBD and other therapeutic alternatives need to be pursued. Probiotics are microbial supplements capable of recolonising the bowel with non-pathogenic strains of bacteria or yeast. Probiotics have long been shown to be beneficial in both infectious and non-infectious digestive disorders. Growing evidence indicates that probiotics may be effective in the treatment of specific clinical IBD conditions. This article addresses the current evidence for the role of enteric flora in the pathogenesis of IBD and the clinical evidence supporting the use of probiotics in specific clinical IBD conditions.

Original languageEnglish (US)
Pages (from-to)179-186
Number of pages8
JournalBioDrugs
Volume17
Issue number3
DOIs
StatePublished - 2003

ASJC Scopus subject areas

  • Biotechnology
  • Pharmacology
  • Pharmacology (medical)

Fingerprint

Dive into the research topics of 'Probiotics and inflammatory bowel disease'. Together they form a unique fingerprint.

Cite this