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

Interaction of Helicobacter pylori with host cells: function of secreted and translocated molecules

Gabriele Rieder1, Wolfgang Fischer, Rainer Haas

  • 1Max von Pettenkofer-Institut, Ludwig-Maximilians-Universität München, Pettenkoferstrasse 9a, 80336 München, Germany.

Current Opinion in Microbiology
|February 8, 2005
PubMed

Insights

Helicobacter pylori uses secreted proteins like VacA and CagA to interact with host cells, causing immunosuppression and altering cell signaling. These virulence factors are key to its survival in the stomach.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Bacteria-host interactions are crucial for understanding pathogenesis.
  • Helicobacter pylori is a gastric pathogen that secretes proteins to survive in the stomach.
  • Key virulence factors include VacA and the cag type-IV secretion system with CagA.

Purpose of the Study:

  • To investigate the role of secreted proteins in Helicobacter pylori pathogenesis.
  • To understand the mechanisms by which VacA and CagA contribute to virulence.

Main Methods:

  • Analysis of secreted and translocated proteins in H. pylori.
  • Investigating the effects of VacA on epithelial and immune cells.
  • Studying the interactions of CagA with eukaryotic signaling molecules.

Main Results:

  • VacA induces immunosuppression in both epithelial and immune cells.
  • CagA interacts with various eukaryotic signaling pathways in a phosphorylation-dependent and -independent manner.
  • H. pylori utilizes a diverse set of secreted proteins for adaptation and virulence.

Conclusions:

  • Secreted proteins, particularly VacA and CagA, are critical for H. pylori's ability to colonize the gastric mucosa and evade host defenses.
  • Understanding these virulence factors provides insights into bacterial pathogenesis and 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

Expression, Purification, and Antimicrobial Activity of S100A1211:10

Expression, Purification, and Antimicrobial Activity of S100A12

Published on: May 13, 2017

Related Concept Videos

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...
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...
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...
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...
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...