Related Experiment Video

Updated: May 2, 2026

In Vitro Assay of Bacterial Adhesion onto Mammalian Epithelial Cells
05:57

In Vitro Assay of Bacterial Adhesion onto Mammalian Epithelial Cells

Published on: May 16, 2011

25.5K

Signal transduction-mediated adherence and entry of Helicobacter pylori into cultured cells

B Su1, S Johansson, M Fällman

  • 1Microbiology and Tumor-Biology Center, Karolinska Institute, Stockholm, Sweden.

Gastroenterology
|August 28, 1999
PubMed
Abstract

Insights

Helicobacter pylori invasion into host cells is mediated by integrins, a process that may contribute to antibiotic resistance. This study investigated the adherence and entry mechanisms of H. pylori into cultured gastric cells.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Helicobacter pylori possesses the ability to invade host cells, potentially conferring resistance to antibiotic treatments.
  • Understanding the mechanisms of H. pylori adherence and entry is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the specific mechanisms underlying the adherence and cellular entry of Helicobacter pylori.
  • To explore the role of integrins in the interaction between H. pylori and gastric cells.

Main Methods:

  • Utilized coinfection with Yersinia expressing YopH tyrosine phosphatase to study H. pylori adherence and entry.
  • Employed inhibitors like genistein and cytochalasin D to block adherence and entry processes.
  • Assessed entry via gentamicin-protection assays and used beta1-integrin-deficient and expressing cell lines.

Main Results:

  • H. pylori induced phosphorylation of proteins similar in size to Yersinia YopH targets.
  • Adherence was inhibited by active YopH, and entry was significantly higher in beta1-integrin-expressing cells.
  • Antibodies against alpha5- and beta1-integrin chains reduced adherence, while genistein and cytochalasin D inhibited entry.

Conclusions:

  • Invasion of gastric epithelial cells by H. pylori occurs through an integrin-mediated pathway.
  • This integrin-dependent invasion mechanism may be key to H. pylori establishing persistent infections in the gastric environment.

More Related Videos

Enteric Bacterial Invasion Of Intestinal Epithelial Cells In Vitro Is Dramatically Enhanced Using a Vertical Diffusion Chamber Model10:52

Enteric Bacterial Invasion Of Intestinal Epithelial Cells In Vitro Is Dramatically Enhanced Using a Vertical Diffusion Chamber Model

Published on: October 22, 2013

13.3K
High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability09:05

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

Related Concept Videos

Adherens Junctions01:24

Adherens Junctions

Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
5.8K
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
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...
2.5K
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...
48
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...
52
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...
44