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The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
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[Pathophysiology of Behçet's disease].

M H Houman1, N Bel Feki1

  • 1Service de médecine interne, hôpital la Rabta, 1007 Tunis, Tunisie; Unité de recherche 02/UR/08-15, faculté de médecine de Tunis, université El Manar 2, Tunis, Tunisie.

La Revue De Medecine Interne
|November 12, 2013
PubMed
Summary

Behçet's disease involves immune system dysregulation in genetically susceptible individuals, potentially triggered by infections like Streptococcus sanguis, leading to inflammation and endothelial dysfunction. Understanding its pathogenesis aids in developing new therapies.

Keywords:
Behçet's diseaseGeneticGénétiqueInfectionLymphocytes T helperMaladie de BehçetPathophysiologiePhysiopathologieT helper lymphocytes

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Area of Science:

  • Immunology
  • Genetics
  • Pathophysiology

Context:

  • Behçet's disease (BD) pathogenesis remains unclear, but involves genetic predisposition and immune system imbalance.
  • Strongest genetic link is HLA-B51; genome-wide association studies identify IL-10, IL-23R, and IL-12RB2 as susceptibility genes.
  • Infectious triggers, possibly Streptococcus sanguis, may initiate disease via molecular mimicry, perpetuating with auto-antigens.

Purpose:

  • To review the current understanding of Behçet's disease etiopathogenesis based on recent scientific advances.
  • To explore the roles of genetic factors, immune responses, and potential triggers in BD development.

Summary:

  • BD pathogenesis involves disrupted immune homeostasis in genetically susceptible individuals, leading to altered innate and adaptive immunity.
  • Key features include pathogenic T cell activation (Th1, Th17 expansion; suppressed Treg), significant roles for cytokines (IL-17, IL-23, IL-21), and endothelial dysfunction.
  • Inflammatory lesions contain neutrophils, CD4(+) T cells, and cytotoxic cells.

Impact:

  • Improved understanding of BD pathophysiology provides a foundation for developing novel and more effective therapeutic strategies.
  • Highlights the complex interplay between genetic susceptibility, immune dysregulation, and potential environmental triggers in Behçet's disease.