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Inflammatory Bowel Disease III: Crohn's Disease

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Chronic Salmonella Infection Induced Intestinal Fibrosis
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Published on: September 22, 2019

Interaction between susceptibility and environment: examples from the digestive tract.

Gerhard Rogler1

  • 1Department of Internal Medicine, Division of Gastroenterology and Hepatology, University Hospital of Zürich, Zürich, Switzerland. gerhard.rogler@usz.ch

Digestive Diseases (Basel, Switzerland)
|July 8, 2011
PubMed
Summary
This summary is machine-generated.

Genetic factors and environmental influences both contribute to inflammatory bowel disease (IBD) risk. Impaired immune responses to gut bacteria in genetically susceptible individuals are key to IBD pathogenesis.

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Area of Science:

  • Gastroenterology and Immunology
  • Genetics and Microbiology

Background:

  • Twin studies indicate a significant genetic component (over 50% concordance in monozygotic twins) for Crohn's disease (CD).
  • The rising incidence of CD and ulcerative colitis (UC) in Western countries suggests environmental factors, or 'Western lifestyle,' trigger disease in susceptible hosts.
  • Genetic susceptibility alone is insufficient, highlighting the crucial role of environmental factors in IBD pathogenesis.

Purpose of the Study:

  • To explore the converging evidence for genetic and environmental factors in inflammatory bowel disease (IBD) pathogenesis.
  • To elucidate the role of specific genes, such as NOD2 and ATG16L1, in the immune response to gut bacteria.
  • To establish a unifying hypothesis for IBD pathophysiology integrating genetic predisposition and environmental triggers.

Main Methods:

  • Analysis of twin study data to estimate genetic heritability of IBD.
  • Review of genetic association studies identifying key susceptibility genes like NOD2 and ATG16L1.
  • Examination of the functional roles of identified genes in innate immunity and bacterial recognition.

Main Results:

  • NOD2, a key gene for CD susceptibility, encodes a receptor that recognizes bacterial products; its common variants are associated with impaired bacterial recognition.
  • The autophagy-related 16-like 1 gene (ATG16L1) is also linked to CD, with its protein product involved in processing intracellular bacteria.
  • Most IBD susceptibility genes are involved in innate immune pathways, primarily the defense against bacteria breaching the intestinal mucosa.

Conclusions:

  • IBD, particularly CD, is increasingly understood as an inadequate immune response to gut bacteria in genetically susceptible individuals.
  • The findings support a unifying concept where genetic susceptibility interacts with environmental factors (e.g., Western lifestyle) to drive chronic intestinal inflammation.
  • Bacteria serve as the critical link connecting environmental exposures to the mucosal immune defense system in IBD.