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Related Concept Videos

Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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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...
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Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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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...
558
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
362
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

344
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.
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Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

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The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
575
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

162
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
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Helicobacter pylori-Induced Decrease in Membrane Expression of Na,K-ATPase Leads to Gastric Injury.

Olga Vagin1,2, Elmira Tokhtaeva1,2, Muriel Larauche2,3

  • 1Department of Pediatrics, DGSOM at UCLA, 10833 LeConte Ave., 12-383 MDCC, Los Angeles, CA 90095, USA.

Biomolecules
|July 27, 2024
PubMed
Summary

Helicobacter pylori infection reduces Na,K-ATPase in gastric cells, impairing the epithelial barrier and causing injury. This study demonstrates the link between reduced Na,K-ATPase and gastric damage.

Keywords:
Helicobacter pyloriNa,K-ATPaseadherens junctionsgastric injuryouabain

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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Pathogen Research

Background:

  • Helicobacter pylori is a common cause of gastric diseases like ulcers and cancer.
  • The exact mechanism of H. pylori-induced gastric injury remains unclear.
  • Na,K-ATPase is crucial for epithelial barrier function in various organs.

Purpose of the Study:

  • To investigate if reduced Na,K-ATPase levels by H. pylori contribute to gastric epithelial injury.
  • To elucidate the role of Na,K-ATPase in maintaining gastric epithelial integrity during H. pylori infection.

Main Methods:

  • Studied human gastric epithelial cells, organoids, and gerbil gastric tissue.
  • Inhibited Na,K-ATPase using ouabain and shRNA silencing.
  • Assessed epithelial barrier function via transepithelial electrical resistance and paracellular permeability.
  • Examined adherens junction organization using E-cadherin immunofluorescence.

Main Results:

  • H. pylori infection and ouabain treatment decreased Na,K-ATPase levels in gastric epithelial cells.
  • Both H. pylori and ouabain impaired epithelial barrier function, increasing permeability.
  • Na,K-ATPase inhibition and H. pylori infection disrupted adherens junctions and E-cadherin organization.
  • shRNA-mediated Na,K-ATPase silencing mimicked these effects in gastric organoids.

Conclusions:

  • The reduction of Na,K-ATPase by H. pylori plays a significant role in gastric epithelial injury.
  • Impaired Na,K-ATPase function compromises the gastric epithelial barrier integrity.
  • This finding contributes to understanding the pathogenesis of H. pylori-associated gastric diseases.