Related Experiment Video

Updated: Aug 19, 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

Induction of host signal transduction pathways by Helicobacter pylori

E D Segal1, C Lange, A Covacci

  • 1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.

Proceedings of the National Academy of Sciences of the United States of America
|July 8, 1997
PubMed

Insights

Helicobacter pylori adherence triggers host cell responses like protein phosphorylation and cytokine release. The cag pathogenicity island (PAI) influences these events, with some pathways independent of tyrosine phosphorylation.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Helicobacter pylori (H. pylori) infection is linked to gastric diseases.
  • Bacterial adherence to gastric cells initiates host responses.
  • The cag pathogenicity island (PAI) is crucial for H. pylori virulence.

Purpose of the Study:

  • To investigate the cellular events associated with H. pylori adherence.
  • To elucidate the role of the cag PAI in host cell signaling and cytokine production.
  • To identify distinct pathways involved in interleukin-8 (IL-8) release.

Main Methods:

  • Cell culture of gastric epithelial cells.
  • Infection with H. pylori strains (wild-type and PAI mutants).
  • Analysis of host cell protein tyrosine phosphorylation.
  • Assessment of cytoskeletal rearrangements (actin, VASP).
  • Quantification of IL-8 release.
  • Kinase inhibition studies.

Main Results:

  • H. pylori adherence induces tyrosine phosphorylation of a 145-kDa protein, actin reorganization, and IL-8 release.
  • Strains with the cag PAI cause distinct cellular events compared to those without.
  • Mutations in PAI genes abolish tyrosine phosphorylation and IL-8 synthesis but not cytoskeletal changes.
  • Two distinct pathways stimulate IL-8 release; one is independent of tyrosine phosphorylation.

Conclusions:

  • H. pylori utilizes the cag PAI to modulate host cell responses.
  • Tyrosine phosphorylation and cytoskeletal changes are separable events in H. pylori-induced signaling.
  • Distinct signaling pathways contribute to IL-8 production, offering potential therapeutic targets.

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

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes08:24

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes

Published on: July 5, 2024

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 to M3...
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...
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 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 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...