Related Experiment Video

Updated: Jun 13, 2026

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

[Relationship between gene polymorphisms in MMP-9 and Helicobacter pylori-related upper gastrointestinal disease in

Qing-Wen Shan1, Cheng-Xue Jing, Lin-Lin Wang

  • 1Department of Pediatrics, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China. shanqw333@yahoo.com.cn

Zhongguo Dang Dai Er Ke Za Zhi = Chinese Journal of Contemporary Pediatrics
|April 27, 2010
PubMed

Insights

Matrix metalloproteinase-9 (MMP-9) gene polymorphisms are not linked to chronic gastritis or duodenal ulcers in children. However, the MMP-9-1562 C/C genotype may increase the risk of Helicobacter pylori infection.

Area of Science:

  • Genetics
  • Pediatric Gastroenterology
  • Microbiology

Background:

  • Helicobacter pylori (H. pylori) infection is a common cause of pediatric gastrointestinal diseases.
  • Matrix metalloproteinase-9 (MMP-9) plays a role in inflammation and tissue remodeling.
  • The association between MMP-9 gene polymorphisms and H. pylori-related conditions in children requires further investigation.

Purpose of the Study:

  • To examine the relationship between MMP-9 gene promoter polymorphisms and susceptibility to H. pylori-related chronic gastritis and duodenal ulcer in children.
  • To assess the influence of these polymorphisms on clinical features of these conditions.

Main Methods:

  • Genotyping of MMP-9-1562C/T gene polymorphisms using PCR-RFLP and sequencing in 100 children with chronic gastritis, 32 with duodenal ulcer, and 102 healthy controls.
  • MMP-9 mRNA expression analysis in gastric mucosa via reverse transcription PCR.

Main Results:

  • No significant differences in genotype distributions or allele frequencies of MMP-9-1562C/T polymorphisms were observed between children with gastrointestinal diseases and healthy controls.
  • Children with chronic gastritis carrying the MMP-9-1562 C/C genotype had a 3.1-fold increased relative risk of H. pylori infection compared to T allele carriers.
  • MMP-9-1562 C/T gene polymorphisms did not impact MMP-9 mRNA expression levels.

Conclusions:

  • MMP-9-1562 C/T gene polymorphisms are not associated with susceptibility to chronic gastritis and duodenal ulcer in the pediatric population.
  • The MMP-9-1562 C/C genotype may be linked to an increased risk of H. pylori infection in children.
Abstract

More Related Videos

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode10:44

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

Published on: June 18, 2016

Quantitative Polymerase Chain Reaction (qPCR)-Based Rapid Diagnosis of Helicobacter pylori Infection and Antibiotic Resistance06:40

Quantitative Polymerase Chain Reaction (qPCR)-Based Rapid Diagnosis of Helicobacter pylori Infection and Antibiotic Resistance

Published on: July 28, 2023

Related Concept Videos

Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Gastritis II: Pathophysiology01:26

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...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer Disease I: Introduction01:25

Peptic Ulcer Disease I: Introduction

Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...
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. Bicarbonate,...
Peptic Ulcer Disease II: Pathophysiology01:24

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...