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Gastritis II: Pathophysiology

Gastritis II: Pathophysiology

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...

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...

Peptic Ulcer Disease IV: Management

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
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Gastritis-II: Pathophysiology

Gastritis-II: Pathophysiology

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.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
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Gastritis can stem from various causes, each...

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Related Experiment Video

Updated: Jun 17, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Published on: October 18, 2018

Prostaglandin E2 prevents Helicobacter-induced gastric preneoplasia and facilitates persistent infection in a mouse

Isabella M Toller¹, Iris Hitzler, Ayca Sayi

¹Institute of Molecular Cancer Research, University of Zürich, Zürich, Switzerland.

Gastroenterology

|December 23, 2009

Summary

Prostaglandin E(2) (PGE(2)) produced by cyclooxygenase-2 (COX-2) plays a key role in Helicobacter pylori infection. PGE(2) suppresses harmful immune responses, preventing gastric cancer precursor lesions.

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Mouse Models Of Helicobacter Infection And Gastric Pathologies

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Evaluation of the Efficacy of the H. pylori Protein HP-NAP as a Therapeutic Tool for Treatment of Bladder Cancer in an Orthotopic Murine Model

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Published on: May 29, 2015

Area of Science:

Gastroenterology
Immunology
Oncology

Background:

Helicobacter pylori infection is a major risk factor for gastric cancer.
Cyclooxygenase-2 (COX-2) and its product prostaglandin E(2) (PGE(2)) are implicated in Helicobacter-induced gastritis and precancerous lesions.

Purpose of the Study:

To investigate the role of COX-2 and PGE(2) in Helicobacter pylori-induced gastritis and gastric cancer precursor lesions.
To elucidate the immunomodulatory effects of PGE(2) on T-helper 1 cell responses during H. pylori infection.

Main Methods:

Utilized mouse models of H. pylori-induced gastric preneoplasia and vaccine-induced protection.
Studied the effects of COX-2 inhibition (celecoxib) and PGE(2) treatment on immune responses and pathology.
Assessed T-helper 1 cell function, cytokine production (interferon-gamma, interleukin-2), and bacterial colonization.

Main Results:

COX-2 and PGE(2) were upregulated during H. pylori infection.
COX-2 inhibition accelerated preneoplasia, while PGE(2) administration prevented and reversed lesions.
PGE(2) exerted protective effects by suppressing T-helper 1 cell effector functions, leading to increased H. pylori colonization.

Conclusions:

COX-2-dependent PGE(2) production is crucial for modulating the immune response during H. pylori infection.
PGE(2) prevents excessive local immune responses and immunopathology by inhibiting pathogenic T-helper 1 cells.
Targeting the COX-2/PGE(2) pathway may offer therapeutic strategies for H. pylori-associated gastric diseases.