Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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. Bicarbonate,...

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

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...

Peptic Ulcer Disease II: Pathophysiology

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.

Peptic Ulcer

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: Pathophysiology

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: Pathophysiology

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...

You might also read

Related Articles

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

Sort by

Same author

Multidisciplinary consensus statement on the clinical management of patients with pancreatic cancer.

Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico·2020

Same author

Corrigendum to "Recommendations from the United European Gastroenterology evidence-based guidelines for the diagnosis and therapy of chronic pancreatitis" [Pancreatology 18(8) (2018) 847-854].

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]·2019

Same author

Platypnea-orthodeoxia syndrome: Importance of patient position for correct diagnosis at the time of (99m)Tc-MAA injection.

Revista espanola de medicina nuclear e imagen molecular·2015

Same author

A Spanish multicenter study to estimate the prevalence and incidence of chronic pancreatitis and its complications.

Revista espanola de enfermedades digestivas·2014

Same author

Early and/or immediately full caloric diet versus standard refeeding in mild acute pancreatitis: a randomized open-label trial.

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]·2014

Same author

Psychological factors are associated with changes in the health-related quality of life in inflammatory bowel disease.

Inflammatory bowel diseases·2013

Search research articles

Related Experiment Video

Updated: Jun 23, 2026

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

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

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

A Hackelsberger¹, U Platzer, M Nilius

¹Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke-University, Magdeburg, Germany.

|November 21, 1998

Summary

Gastric mucosal surface hydrophobicity (GMSH) decreases with age, independent of H. pylori infection. This age-related decline in GMSH may increase ulcer risk in older adults, potentially interacting with H. pylori and NSAIDs.

More Related Videos

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

Published on: June 18, 2016

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

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

Published on: March 7, 2025

Related Experiment Videos

Last Updated: Jun 23, 2026

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

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

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

Published on: June 18, 2016

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

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

Published on: March 7, 2025

Area of Science:

Gastroenterology and Internal Medicine
Mucosal Immunology
Aging Research

Background:

Gastric mucosal surface hydrophobicity (GMSH) is a key defense mechanism against gastric injury.
GMSH is compromised by Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs).
Gastric ulcers are more prevalent in the elderly, suggesting reduced mucosal resistance.

Purpose of the Study:

To determine if aging physiologically reduces GMSH.
To investigate the relationship between GMSH, aging, and H. pylori infection.

Main Methods:

120 patients without peptic ulcer disease were stratified into three age groups.
Gastric biopsy specimens were analyzed for histology, H. pylori (urease test, immunoblotting), and GMSH via contact angle measurement.
GMSH was measured at antrum, corpus, and cardia biopsy sites.

Main Results:

GMSH was significantly lower in H. pylori-infected individuals (p=0.0001).
GMSH decreased with age independently of H. pylori status (p=0.0001).
Antral GMSH was higher than corpus GMSH in both infected and uninfected patients.

Conclusions:

Physiological aging reduces GMSH, potentially increasing ulcer risk in the elderly.
The decline in GMSH with age may synergize with H. pylori and NSAIDs to impair gastric mucosal defense.