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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.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...

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...

Gastritis-I: Introduction and Types

Gastritis-I: Introduction and Types

Gastritis, defined by the inflammation or irritation of the stomach lining or gastric mucosa, manifests in several distinct forms: acute, chronic, reactive, and a specific subtype known as autoimmune metaplastic atrophic gastritis.
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...

Inflammatory Bowel Disease III: Crohn's Disease

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...

Irritable Bowel Syndrome I: Introduction

Irritable Bowel Syndrome I: Introduction

Irritable Bowel Syndrome (IBS) is characterized by functional disturbances in the gastrointestinal system, presenting a cluster of symptoms without evident structural or biochemical abnormalities. It primarily affects the large intestine and may cause abdominal pain, bloating, excessive gas, diarrhea, constipation, or both.
IBS is a chronic condition that can persist over a long period or recur frequently.
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Causal Relationship Between 91 Inflammatory Factors and Gastritis: A Two-Sample Bidirectional Mendelian Randomization

Tong Wang^1,2, Lu Lin^1,2

¹Department of Clinical Laboratory, The Fourth People's Hospital of Chengdu, Sichuan province, China.

Current Molecular Medicine

|June 19, 2026

Summary

This summary is machine-generated.

This study used Mendelian Randomization to investigate inflammation

Keywords:

Mendelian randomization acute gastritis causality relationship chronic gastritis inflammation.inflammatory factors

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Area of Science:

Gastroenterology
Immunology
Genetics

Background:

Inflammation is implicated in gastrointestinal diseases.
Causal links between inflammation and gastritis require validation.

Purpose of the Study:

To evaluate the causal effects of inflammatory factors on gastritis using Mendelian Randomization.
To identify potential biomarkers for acute and chronic gastritis.

Main Methods:

Mendelian Randomization analysis utilizing GWAS and FinnGen databases.
Assessment of 91 inflammatory factors for association with acute and chronic gastritis.
Statistical tests for heterogeneity (Cochran's Q) and pleiotropy (MR-Egger's intercept).

Main Results:

Identified specific inflammatory factors associated with acute gastritis (Axin-1, CXCL10, Fms-related tyrosine kinase 3 ligand).
Linked distinct factors to chronic gastritis (CXCL10, GDNF, LIFR, HGF, FGF19).
Reverse MR showed chronic gastritis downregulates specific inflammatory factors (e.g., LIFR, IL-2Rβ).

Conclusions:

Acute and chronic gastritis involve distinct inflammatory profiles.
Chronic gastritis can inversely affect inflammatory factor levels.
CXCL10 and LIFR show potential as gastritis biomarkers.