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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 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...
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.
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...
Microbiota of the Stomach and Small Intestine01:27

Microbiota of the Stomach and Small Intestine

The human gastrointestinal (GI) tract is characterized by distinct physicochemical conditions that shape its microbial communities. Among these, the stomach presents a particularly challenging environment for microbial colonization due to its highly acidic pH, ranging from 1 to 3. This extreme acidity effectively limits microbial density. However, certain acid-tolerant microorganisms are capable of surviving in this niche. Notably, Helicobacter pylori can colonize the gastric mucosa,...

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Related Experiment Video

Updated: Jun 20, 2026

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
11:48

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration

Published on: May 7, 2018

Helicobacter pylori and microcirculation.

Hidekazu Suzuki1, Masayuki Suzuki, Hiroyuki Imaeda

  • 1Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. hsuzuki@sc.itc.keio.ac.jp

Microcirculation (New York, N.Y. : 1994)
|August 27, 2009
PubMed
Summary

Helicobacter pylori (Hp) infection impacts microcirculation, leading to various disorders. This review details Hp

Area of Science:

  • Gastroenterology and Microbiology
  • Pathophysiology
  • Vascular Biology

Background:

  • Helicobacter pylori (Hp) infection is a significant global health concern.
  • While Hp infection kinetics are well-studied, its impact on microcirculation remains less explored.
  • Microcirculation is a key target in the pathogenesis of Hp-induced disorders.

Purpose of the Study:

  • To review recent developments in understanding the pathophysiology of Hp-induced disorders.
  • To focus on the critical role of microcirculation in Hp pathogenesis.
  • To summarize current knowledge on microcirculatory aspects of Hp infection.

Main Methods:

  • Systematic review of animal and human studies.
  • Identification and analysis of published data on microcirculatory aspects of Hp infection.

More Related Videos

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
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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

Related Experiment Videos

Last Updated: Jun 20, 2026

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
11:48

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration

Published on: May 7, 2018

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

  • Synthesis of information on pathophysiology and therapeutic strategies.

    • Main Results:

    • Microcirculation is demonstrably affected by Helicobacter pylori (Hp) infection.
    • Hp infection contributes to both gastric and extragastric sequelae.
    • Understanding microcirculatory changes is crucial for disease elucidation.

    Conclusions:

    • This review highlights the significant role of microcirculation in Hp-induced pathophysiology.
    • It identifies potential approaches to further clarify gastric and extragastric sequelae.
    • It suggests avenues for developing targeted therapeutic strategies against Hp infection.