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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 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 III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
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...
Pulmonary Tuberculosis II01:28

Pulmonary Tuberculosis II

Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

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...

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Updated: May 19, 2026

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
10:44

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

Published on: June 18, 2016

Urease and Helicobacter spp. antigens in pulmonary granuloma.

B Herndon1, T Quinn, N Wasson

  • 1Pulmonary Research Laboratory, University of Missouri-Kansas City School of Medicine, Kansas City, MO, USA. Herndonb@umkc.edu

Journal of Comparative Pathology
|August 21, 2012
PubMed
Summary
This summary is machine-generated.

A novel rat model suggests Helicobacter pylori urease may cause pulmonary sarcoidosis through esophageal reflux. This research offers insights into the origins of this human lung disease.

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One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
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Published on: April 6, 2015

Area of Science:

  • Immunology
  • Pulmonology
  • Microbiology

Background:

  • Pulmonary sarcoidosis is a human disease with an unknown cause and no existing animal model.
  • Patients with sarcoidosis exhibit serum antibodies against Helicobacter pylori and its urease enzyme.
  • Helicobacter pylori urease may reach the lungs via esophageal reflux, as the bacteria cannot survive in the pulmonary environment.

Purpose of the Study:

  • To establish and utilize a rat model to investigate the gastro-esophageal reflux of urease into the airways.
  • To compare the pathology observed in the rat model with tissues from human sarcoidosis patients.
  • To explore potential insights into the pathogenesis of pulmonary diseases linked to Helicobacter species.

Main Methods:

  • A rat model was developed to simulate gastro-esophageal reflux of urease.
  • Pathological analysis of rat lung tissues and comparison with human sarcoidosis patient tissues.
  • Intratracheal and intravenous administration of urease protein (alone and coupled to microbeads) in rats.
  • Measurement of biomarkers such as interleukin-1β and platelet-activating factor.

Main Results:

  • The rat model exhibited peribronchial lymphocytic infiltration, a feature seen in human sarcoidosis.
  • Granulomas, characteristic of sarcoidosis, were observed in rat lungs, particularly after intravenous urease administration.
  • Key sarcoidosis biomarkers, including interleukin-1β and platelet-activating factor, were acutely upregulated in the rat model.

Conclusions:

  • The developed rat model shows promise for studying pulmonary sarcoidosis pathogenesis.
  • Urease, potentially from Helicobacter pylori via reflux, may play a role in sarcoidosis development.
  • Further research using this model could illuminate the origins of pulmonary diseases in humans and other species harboring gastric Helicobacter spp.