Related Experiment Video

Updated: Aug 9, 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

Helicobacter pylori infection is the major risk factor for gastric inflammation in the cardia

Yasuo Egi1, Sunjin Kim, Masanori Ito

  • 1Department of Medicine and Molecular Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.

Digestive Diseases and Sciences
|April 8, 2006
PubMed

Insights

Helicobacter pylori infection is a significant risk factor for cardiac inflammation in the gastric cardia, particularly in Japanese populations. This finding was confirmed through histological analysis and magnifying gastroscopy.

Area of Science:

  • Gastroenterology
  • Pathogenesis Research
  • Microbiology

Background:

  • Gastric inflammation in the cardia is a condition requiring further etiological clarification.
  • Understanding the pathogenesis of cardiac inflammation is crucial for effective treatment strategies.

Purpose of the Study:

  • To elucidate the pathogenesis of gastric inflammation in the cardia.
  • To identify key risk factors associated with cardiac inflammation in a Japanese cohort.

Main Methods:

  • Histological evaluation of biopsy specimens from the gastric antrum, corpus, and cardia.
  • Magnifying gastroscopy to assess cardiac inflammation.
  • Analysis of Helicobacter pylori infection, gastric pH, bile acid levels, serum pepsinogen and gastrin, GERD, and smoking habits.

Main Results:

  • A statistically significant higher prevalence of H. pylori infection was observed in patients with cardiac inflammation (P < 0.05).
  • Cardiac inflammation correlated with low gastric acid output but not with bile acid concentration or smoking.
  • Cardiac inflammation was more pronounced in individuals without gastroesophageal reflux disease (GERD).

Conclusions:

  • Helicobacter pylori infection is identified as a major risk factor for cardiac inflammation in the Japanese population.
  • The study highlights the role of H. pylori in the pathogenesis of cardiac inflammation, independent of GERD status.

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...
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...
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 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...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.