Cited by 319Gut microbiota and healthInflammatory Bowel DiseaseProbiotics and Fermented Foods

Commensal bacteria, traditional and opportunistic pathogens, dysbiosis and bacterial killing in inflammatory bowel diseases

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Packey, Christopher D, Sartor, R Balfour·2009·Current Opinion in Infectious Diseases

Abstract

PURPOSE OF REVIEW: The authors present evidence published during the past 2 years of the roles of commensal and pathogenic bacteria in the pathogenesis of the inflammatory bowel diseases. RECENT FINDINGS: Rodent models conclusively implicate commensal enteric bacteria in chronic, immune-mediated, experimental colitis, and genetically determined defects in bacterial killing by innate immune cells are found in a subset of patients with Crohn's disease. There is no evidence that a single pathogen, including Mycobacterium avium subspecies paratuberculosis, causes Crohn's disease or ulcerative colitis. However, adherent/invasive Escherichia coli are associated with ileal Crohn's disease, with the mechanisms and genetics of adherent/invasive E. coli virulence being elucidated. Molecular characterization of the microbiota in patients with inflammatory bowel diseases reveals decreased biodiversity of commensal bacteria, most notably the phyla Bacteroidetes and Firmicutes, including the clinically relevant Faecalibacterium prausnitzii, and increased E. coli concentrations. VSL#3 is one probiotic preparation shown to be efficacious in certain clinical situations in small clinical trials. SUMMARY: Further characterization of altered microbiota in patients with inflammatory bowel diseases and linking dysbiosis with host genetic alterations in immunoregulation, innate microbial killing and barrier function are critical, so that individualized treatments to increase beneficial commensals and their metabolic products (probiotic and prebiotic administration) and diminish deleterious species such as adherent/invasive E. coli can be tailored for defined patient subsets.

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  1. [41]Liu B Schmitz JM Holt LC Increased intracellular survival of E. coli NC101 within macrophages may contribute to its ability to induce colitis Gastroenterology 2009 in press (abstract)

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Authors
Packey, C. D., & Sartor, R. B.
Affiliations
University of North Carolina at Chapel Hill (US)
Corresponding author
Sartor, R Balfour
Venue
Current Opinion in Infectious Diseases
Published
2009-06
Volume
22
Issue
3
Pages
292-301
ISSN
0951-7375 (ISSN-L)
OpenAlex
W1978636470
Cited by
319
References
83
Citations by year
2026: 5 · 2025: 4 · 2024: 12 · 2023: 11 · 2022: 11 · 2021: 14 · 2020: 15 · 2019: 25 · 2018: 16 · 2017: 13 · 2016: 30 · 2015: 15 · 2014: 30 · 2013: 21 · 2012: 34
FWCI
2.47
Type
journal article
Language
en
Open access
Locations
  • Current Opinion in Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK53347, R01DK040249, R01 DK 40249, P30‐DK34987, R01DK053347, P30DK034987, T32DK007737)
  • National Center for Research Resources (P40RR018603)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
Keywords
inflammatory bowel disease, Crohn's disease, ulcerative colitis, commensal bacteria, dysbiosis, gut microbiota, adherent-invasive Escherichia coli, Mycobacterium avium subsp. paratuberculosis, Faecalibacterium prausnitzii, Bacteroidetes, Firmicutes, probiotics, VSL#3, prebiotics, experimental colitis, host genetic susceptibility
MeSH terms
Bacteria, Humans, Inflammatory Bowel Diseases, Immunity, Mucosal, Probiotics, Gastrointestinal Tract, Biodiversity

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