Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

2.5K
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...
2.5K
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

1.6K
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.
1.6K
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

2.3K
In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
2.3K
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

2.9K
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.
2.9K
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

36
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...
36
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

1.6K
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
1.6K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Esophageal Lichen Planus: Highlighting Diagnostic Challenges and Therapeutic Limitations.

ACG case reports journal·2026
Same author

An IL-17-DUOX2 axis controls gastrointestinal colonization by Candida albicans.

Nature communications·2026
Same author

Luminal LPS is transported across murine small intestine by a caveolin-1 dependent endocytic mechanism induced by chronic feeding of a Western-style diet.

Gut microbes·2025
Same author

Lipopolysaccharide transport during long-chain fatty acid exposure is mediated by caveolin-1 dependent endocytosis in murine jejunum.

Tissue barriers·2025
Same author

Alteration of the microbiota with vancomycin and high-fiber diet affects short-chain fatty acid/free fatty acid receptor signaling in rat caecum.

The Journal of nutritional biochemistry·2025
Same author

Restraint stress exacerbates indomethacin-induced gastric antral ulcers by gastroparesis via activation of corticotropin-releasing factor 2 receptors in refed mice.

The Journal of pharmacology and experimental therapeutics·2025

Related Experiment Video

Updated: Apr 23, 2026

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging
05:10

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

664

Gastroduodenal mucosal defense.

Thomas Kemmerly1, Jonathan D Kaunitz

  • 1aCedars-Sinai Medical Residency Program bGreater Los Angeles Veteran Affairs Healthcare System, WLAVA Medical Center cDepartments of Medicine and Surgery, UCLA School of Medicine dDepartment of Medicine, CURE: Digestive Diseases Research Center eBrentwood Biomedical Research Institute, Los Angeles, California, USA.

Current Opinion in Gastroenterology
|September 18, 2014
PubMed
Summary

Recent research deepens understanding of gastroduodenal mucosal defense mechanisms. New findings highlight novel proteins and processes, offering potential therapeutic targets for gastrointestinal health.

More Related Videos

Surgical Models of Gastroesophageal Reflux with Mice
05:19

Surgical Models of Gastroesophageal Reflux with Mice

Published on: August 25, 2015

10.1K
Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection
08:24

Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection

Published on: July 5, 2024

1.2K

Related Experiment Videos

Last Updated: Apr 23, 2026

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging
05:10

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

664
Surgical Models of Gastroesophageal Reflux with Mice
05:19

Surgical Models of Gastroesophageal Reflux with Mice

Published on: August 25, 2015

10.1K
Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection
08:24

Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection

Published on: July 5, 2024

1.2K

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Immunology

Background:

  • Gastroduodenal mucosal defense is crucial for maintaining gastrointestinal health.
  • Understanding the molecular mechanisms of mucosal protection and healing is an ongoing area of research.

Purpose of the Study:

  • To review recent developments in the field of gastroduodenal mucosal defense.
  • To identify new molecular mechanisms, proteins, and processes involved in mucosal protection.

Main Methods:

  • Literature review of research published over the past year.
  • Focus on molecular mechanisms, cellular-level healing, and protective factors.

Main Results:

  • Continued elucidation of known mediators like nitric oxide, toll-like receptors (TLRs), nucleotide-binding oligomerization domain-containing proteins (NOD2), beta-defensins, macrophages, dendritic cells, mucins, and autophagy.
  • Identification of novel mediators including dual oxidases, defense against radiation injuries, and proteins like ZBP-89.
  • Exploration of the influence of aging and diet on mucosal defense.

Conclusions:

  • Recent findings enhance the understanding of gastroduodenal defense mechanisms.
  • New discoveries suggest innovative research directions.
  • Potential novel therapeutic targets for gastroduodenal disorders have been identified.