How does Helicobacter pylori cause mucosal damage? The inflammatory response
P B Ernst1, S E Crowe, V E Reyes
1Department of Pediatrics (Child Health Research Center), University of Texas Medical Branch, Galveston, USA.
Gastroenterology
|December 12, 1997
Summary
Helicobacter pylori infection outcomes vary due to host factors. Understanding the host immune response is key to preventing gastric diseases like ulcers and cancer.
Area of Science:
- Gastroenterology and Immunology
- Microbial Pathogenesis
Background:
- Helicobacter pylori infection affects a subset of individuals, leading to peptic ulcers or gastric cancer.
- Host immune and inflammatory responses are critical in determining disease outcomes.
- The ideal host response clears infection without causing self-damaging inflammation.
Purpose of the Study:
- To explore protective mucosal immune responses.
- To compare H. pylori-induced gastric immune responses to the ideal scenario.
- To investigate the role of these responses in autoimmune damage and potential for immunomodulation via vaccination.
Main Methods:
- This review synthesizes current research on host-pathogen interactions in H. pylori infection.
- It examines immunological mechanisms underlying gastric disease development.
- The review discusses potential therapeutic strategies targeting immune responses.
Main Results:
- Gastric immune responses during H. pylori infection often deviate from protective, non-damaging patterns.
- These aberrant responses may contribute to autoimmune-mediated gastric tissue damage.
- Vaccination strategies are being explored to modulate immune responses towards a protective phenotype.
Conclusions:
- Host immune responses play a pivotal role in H. pylori-associated gastric diseases.
- Aberrant inflammation during infection can lead to pathology and potentially autoimmunity.
- Targeting and modulating these immune responses, possibly through vaccination, offers a promising avenue for prevention and treatment.
Related Concept Videos
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
1.6K
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...
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...
1.6K
01:17Gastritis-II: Pathophysiology
1.9K
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...
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...
1.9K
01:28Peptic Ulcer Disease II: Pathophysiology
3.0K
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.
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.
3.0K
01:27Peptic Ulcer
48
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...
48
01:26Gastritis II: Pathophysiology
52
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...
52
01:24Peptic Ulcer Disease II: Pathophysiology
44
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...
44