Related Experiment Video

Updated: Apr 16, 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

16.2K

Helicobacter pylori interferes with leukocyte migration via the outer membrane protein HopQ and via CagA

Benjamin Busch1, Ramona Weimer1, Christine Woischke1

  • 1Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Ludwig-Maximilians-Universität, München, Germany.

International Journal of Medical Microbiology : IJMM
|March 5, 2015
PubMed

Insights

Helicobacter pylori infection impairs immune cell movement. This bacterial pathogen inhibits granulocyte migration, a process dependent on its CagA protein, impacting chronic infection dynamics.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Helicobacter pylori is a human gastric pathogen known for causing chronic infections.
  • H. pylori employs immune evasion strategies, including avoiding Toll-like receptor recognition and modulating T cell responses.
  • Previous studies detailed H. pylori interactions with immune cells, focusing on activation, cytokine release, and oxidative burst.

Purpose of the Study:

  • To investigate the effect of H. pylori infection on human granulocyte migration.
  • To determine the role of specific H. pylori virulence factors, including the cag pathogenicity island and CagA, in modulating immune cell migration.

Main Methods:

  • Infection of human granulocytes and differentiated HL-60 cells (dHL-60 cells) with H. pylori.
  • Assessment of cell migration using three-dimensional collagen gel and under agarose assays.
  • Utilized complemented H. pylori strains producing phosphorylation-resistant or cleavage-resistant CagA variants.

Main Results:

  • H. pylori infection inhibited dHL-60 cell migration in both tested conditions.
  • Migration inhibition in collagen gel was independent of the cag pathogenicity island.
  • Migration inhibition in the under agarose assay required the cag pathogenicity island, CagA, and HopQ, with CagA tyrosine phosphorylation being essential but processing not required.

Conclusions:

  • H. pylori directly interferes with the migratory behavior of immune cells, specifically granulocytes.
  • The cag pathogenicity island and its effector CagA play a crucial role in H. pylori-mediated inhibition of immune cell migration.
  • Tyrosine phosphorylation of CagA is critical for this migration inhibition, suggesting a novel mechanism of immune subversion by H. pylori.
Keywords:
CagAGranulocytesHelicobacter pyloriHopQLeukocyte migrationfMLP

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

10.3K
Mouse Models Of Helicobacter Infection And Gastric Pathologies07:43

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Published on: October 18, 2018

23.5K

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...
36
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...
2.4K
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
Colonisation of Pathogens01:25

Colonisation of Pathogens

Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...
63
Chemotaxis in E. coli01:27

Chemotaxis in E. coli

Chemotaxis in Escherichia coli is a sensory-driven motility mechanism that enables bacteria to navigate chemical gradients, moving toward beneficial environments while avoiding harmful conditions. This process relies on a signal transduction system integrating external chemical cues with flagellar motor control.Chemoreceptors and Signal DetectionE. coli detects chemical gradients through methyl-accepting chemotaxis proteins (MCPs), which are membrane-bound chemoreceptors that sense attractants...
1.4K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
8.4K