Related Experiment Video

Updated: May 6, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
09:05

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

15.1K

Interleukin 1beta induces gastric epithelial cell matrix metalloproteinase secretion and activation during

M Gööz1, M Shaker, P Gööz

  • 1Gastroenterology and Hepatology Division, Department of Medicine, Medical University of South Carolina, Charleston, SC, USA.

Gut
|August 13, 2003
PubMed
Abstract

Insights

Interleukin-1beta (IL-1beta) stimulates gastric epithelial cells to secrete matrix metalloproteinase-3 (MMP-3), contributing to tissue damage during Helicobacter pylori infections. However, H. pylori requires additional factors for a complete MMP-3 response.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Immunology

Background:

  • Matrix metalloproteinases (MMPs) are key enzymes in tissue remodeling and inflammation.
  • Helicobacter pylori infection elevates epithelial MMP-1 and MMP-3 secretion.
  • The role of IL-1beta in H. pylori-induced MMP secretion requires further characterization.

Purpose of the Study:

  • To investigate the role of IL-1beta in Helicobacter pylori-induced matrix metalloproteinase secretion by gastric epithelial cells.
  • To elucidate the specific MMPs involved in this host-pathogen interaction.

Main Methods:

  • Human gastric adenocarcinoma (AGS) cells were treated with H. pylori and/or IL-1beta.
  • Enzyme-linked immunosorbent assay (ELISA) measured IL-8 secretion.
  • Caseinolytic activity and MMP-3 specific immunoblots analyzed MMP activity and presence.

Main Results:

  • Both IL-1beta and H. pylori induced significant IL-8 secretion and caseinolytic activity.
  • IL-1beta primarily induced a MMP-3/TIMP-3 heterodimer, while H. pylori increased both this heterodimer and active MMP-3.
  • H. pylori stimulated 24-fold greater MMP-3 activity compared to IL-1beta alone, indicating a strong interaction.

Conclusions:

  • IL-1beta directly stimulates gastric epithelial MMP-3 secretion, contributing to tissue damage in H. pylori infections.
  • H. pylori infection elicits a more comprehensive MMP-3 secretory response than IL-1beta alone.
  • Additional bacterial or host factors are involved in the full MMP-3 response to H. pylori.

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

19.9K
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

1.2K

Related Concept Videos

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...
1.6K
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...
1.9K
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
3.0K
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...
50
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...
87
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...
76