What is pathogenensis of inflammatory bowel disease?

 Pathogenesis of Inflammatory Bowel Disease (IBD)

The pathogenesis of Inflammatory Bowel Disease (IBD)—which includes Crohn’s disease and ulcerative colitis—is complex and multifactorial. It involves a combination of genetic predisposition, environmental triggers, dysregulation of the immune system, and alterations in the gut microbiome.



Here's a detailed breakdown of the key mechanisms involved:

 1. Genetic Susceptibility

  • IBD tends to run in families, indicating a strong genetic component.

  • Over 200 genetic loci have been associated with IBD, especially:

    • NOD2 gene mutations (strongly linked with Crohn’s disease)

    • IL23R, ATG16L1, and other genes affecting immune response and autophagy

  • These mutations impair the immune system’s ability to handle intestinal bacteria properly.

 2. Immune System Dysregulation

  • In IBD, the immune system overreacts to harmless gut microbes or self-antigens.

  • This results in chronic inflammation of the intestinal lining.

Key Immune Players:

  • Innate immunity: Defects in mucosal barriers and antigen presentation

  • Adaptive immunity:

    • Th1 and Th17 responses are predominant in Crohn’s disease.

    • Th2-like responses are more common in ulcerative colitis.

The immune system mistakenly attacks intestinal cells, leading to tissue injury and inflammation.

 3. Altered Gut Microbiota (Dysbiosis)

  • Healthy individuals have a balanced microbiome that protects the gut lining.

  • IBD patients show a reduction in beneficial bacteria (e.g., Faecalibacterium prausnitzii) and an increase in harmful microbes.

  • This microbial imbalance triggers inflammation by:

    • Stimulating immune cells

    • Disrupting the mucosal barrier

4. Environmental Factors

Several external factors may trigger IBD in genetically predisposed individuals:

  • Diet (high fat, low fiber, processed foods)

  • Smoking (risk factor for Crohn’s disease; protective in ulcerative colitis)

  • Antibiotic use (alters gut flora)

  • Infections (viral or bacterial gastroenteritis)

  • Urban living and stress may also increase susceptibility.

5. Defective Epithelial Barrier

  • The intestinal epithelial layer forms a barrier to protect underlying tissues from microbes and toxins.

  • In IBD:

    • Tight junctions between epithelial cells are weakened.

    • This allows bacteria and antigens to penetrate the mucosa.

    • Resulting in further immune activation and chronic inflammation.

Summary of Pathogenic Mechanism:

  1. Genetic mutation → impaired microbial recognition and immune regulation

  2. Environmental trigger → alters gut microbiota and epithelial barrier

  3. Microbial dysbiosis + barrier defects → antigen exposure

  4. Immune system activation → chronic intestinal inflammation


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