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Gastritis-II: Pathophysiology01:17

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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
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Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
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Local type 2 immunity in eosinophilic gastritis.

Netali Ben-Baruch Morgenstern1, Tetsuo Shoda1, Yrina Rochman1

  • 1Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.

The Journal of Allergy and Clinical Immunology
|February 8, 2023
PubMed
Summary
This summary is machine-generated.

Eosinophilic gastritis (EoG) involves increased T helper 2 (TH2) cells and type 2 cytokines. These TH2 cells correlate strongly with EoG pathology, indicating their role in disease.

Keywords:
Eosinophilic gastritisT cellseosinophilstype 2 cytokines

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cellular Biology

Background:

  • Eosinophilic gastritis (EoG) is linked to type 2 immunity.
  • The cellular sources of type 2 cytokines and gastric T-cell composition in EoG are not well understood.
  • The relationship between gastric T cells and disease pathology requires further investigation.

Purpose of the Study:

  • To define gastric T-cell populations in EoG.
  • To investigate the association between gastric T cells and EoG pathology.
  • To explore the role of T helper 2 (TH2) cells and type 2 cytokines in EoG.

Main Methods:

  • Gastric biopsy samples from EoG patients and controls were analyzed using histology, endoscopy, and flow cytometry.
  • T-cell populations, including regulatory T cells and TH2 cells, were quantified.
  • In a separate cohort, mRNA levels of IL-4, IL-5, and IL-13 were correlated with EoG pathologic parameters.

Main Results:

  • Gastric T cells in EoG included increased regulatory T cells and TH2 cells (CD3+CD4+GATA3+) compared to controls.
  • TH2 cell levels significantly correlated with gastric eosinophil counts, endoscopic findings, and histopathology.
  • Elevated IL-4, IL-5, and IL-13 mRNA levels in EoG also correlated with disease severity.

Conclusions:

  • Eosinophilic gastritis is associated with an increase in gastric T helper 2 (TH2) cells.
  • These TH2 cells produce type 2 cytokines and their levels strongly correlate with EoG disease pathology.
  • The findings highlight the central role of TH2 cells in the pathogenesis of EoG.