Related Experiment Video

Updated: Nov 25, 2025

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
05:23

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

611

Helicobacter pylori Infection and the Patterns of Gastric Mucin Expression in Children

Ana-Maria Teodora Domșa1, Raluca Lupușoru2,3, Dan Gheban1,4

  • 1Department of Pathology, "Iuliu Hațieganu" University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania.

Journal of Clinical Medicine
|December 16, 2020
PubMed

Insights

Helicobacter pylori infection alters mucin expression in children, with lower MUC5AC and higher MUC2 levels observed. Chronic inflammation also impacts MUC6 and MUC2 expression, suggesting a role in pediatric gastric health.

Area of Science:

  • Pediatric Gastroenterology
  • Molecular Gastric Pathology
  • Microbiome-Host Interactions

Background:

  • Helicobacter pylori (H. pylori) is a known risk factor in gastric carcinogenesis.
  • H. pylori infection alters gastric mucin expression in adults.
  • Understanding these alterations in children is crucial for early detection and prevention.

Purpose of the Study:

  • To investigate the impact of H. pylori infection on secretory mucin expression in the pediatric antral mucosa.
  • To compare mucin expression patterns between H. pylori-infected and non-infected children.

Main Methods:

  • Immunohistochemical staining of pediatric antral biopsy slides for MUC5AC, MUC6, and MUC2.
  • Digitalization and both semiquantitative and quantitative scoring of mucin expression.
  • Analysis of mucin expression in relation to H. pylori infection status and chronic inflammation.

Main Results:

  • MUC5AC expression was significantly reduced in H. pylori-infected children.
  • MUC2 expression was notably increased in infected children.
  • MUC6 expression did not differ between infected and non-infected groups, but was altered by chronic inflammation and associated with gastric atrophy.

Conclusions:

  • H. pylori infection influences specific mucin expressions in pediatric gastric mucosa.
  • Chronic inflammation plays a role in altering mucin profiles, particularly MUC6 and MUC2.
  • Further research is needed to elucidate age-specific patterns and the role of H. pylori-mucin interactions in gastric carcinogenesis.
Abstract

Keywords:
Helicobacter pylorichildrengastric mucinsgastritisimmunohistochemistry

More Related Videos

Mouse Models Of Helicobacter Infection And Gastric Pathologies07:43

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Published on: October 18, 2018

21.5K
Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection08:24

Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection

Published on: July 5, 2024

924

Related Concept Videos

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
355
Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
1.4K
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

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...
767
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

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...
906
Gastritis-II: Pathophysiology01:17

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...
899
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
936