Related Experiment Video

Updated: Aug 7, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies
07:43

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Published on: October 18, 2018

Infiltration of Helicobacter pylori in the gastric mucosa

Nirag C Jhala1, Gene P Siegal, Katrin Klemm

  • 1Department of Pathology, University of Alabama at Birmingham, 619, 6th Ave S, Birmingham, AL 35233, USA.

American Journal of Clinical Pathology
|January 11, 2003
PubMed

Insights

Helicobacter pylori can invade the stomach's lamina propria, explaining its inflammatory cell recruitment. This study provides morphologic evidence of H. pylori invasive capability using advanced microscopy techniques.

Area of Science:

  • Gastroenterology
  • Microbiology
  • Pathology

Background:

  • Helicobacter pylori infection is a major cause of gastritis and peptic ulcers.
  • The mechanism by which H. pylori recruits inflammatory cells to the gastric mucosa is not fully understood.
  • Previous studies have primarily focused on H. pylori presence on the mucosal surface.

Purpose of the Study:

  • To investigate the invasive potential of Helicobacter pylori into the gastric lamina propria.
  • To determine if H. pylori presence in the lamina propria correlates with gastric inflammation.
  • To provide morphologic evidence of H. pylori's invasive capability.

Main Methods:

  • Immunohistochemical staining (Warthin-Starry silver and immunoperoxidase) of 67 gastric biopsy specimens for H. pylori.
  • Transmission electron microscopy (TEM) on one case to confirm findings.
  • Statistical analysis to correlate H. pylori presence with inflammation levels.

Main Results:

  • H. pylori was detected in the lamina propria of 30% (20/67) of gastric biopsy specimens using immunohistochemistry.
  • Warthin-Starry silver stain alone failed to identify H. pylori in the lamina propria.
  • TEM confirmed the presence of H. pylori within the lamina propria.
  • Surface H. pylori presence was significantly associated with both active (P < .0001) and chronic (P < .0001) inflammation.

Conclusions:

  • Helicobacter pylori can actively infiltrate the gastric lamina propria.
  • This invasion provides a potential mechanism for H. pylori-induced inflammatory cell recruitment.
  • Morphologic evidence supports H. pylori's invasive capability beyond the mucosal surface.

More Related Videos

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

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance05:23

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

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...
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...
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...