Neutrophil activation by Helicobacter pylori
C Mooney1, J Keenan, D Munster
1University Department of Surgery, Christchurch School of Medicine, New Zealand.
Gut
|August 1, 1991
Summary
Helicobacter pylori secretes a substance, likely N-formyl-methionyl-leucyl-phenylalanine (FMLP), that activates human polymorphonuclear leukocytes (PMNLs). Immune complexes of H. pylori and antibodies further enhance this PMNL activation, potentially causing gastritis.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Helicobacter pylori infection leads to persistent polymorphonuclear leukocyte (PMNL) infiltration in the gastric mucosa.
- Understanding the interaction between H. pylori and host immune cells is crucial for explaining associated gastritis.
Purpose of the Study:
- To investigate the activation of human PMNLs by substances produced by H. pylori.
- To determine the role of H. pylori-derived products and immune complexes in PMNL activation and gastric inflammation.
Main Methods:
- Stimulation of human PMNLs with filtered H. pylori conditioned media and purified H. pylori components.
- Measurement of PMNL oxidative burst response.
- High-pressure liquid chromatography (HPLC) to identify active substances.
- Evaluation of the effect of H. pylori opsonized with anti-H. pylori plasma on PMNL activation.
Main Results:
- Filtered H. pylori conditioned media induced a significant PMNL oxidative burst, comparable to N-formyl-methionyl-leucyl-phenylalanine (FMLP).
- A fraction from H. pylori extract stimulated PMNLs and cross-reacted antigenically with FMLP.
- Opsonized H. pylori prolonged the FMLP-induced oxidative burst, while unopsonized bacteria did not significantly activate PMNLs.
- Combined H. pylori conditioned media and anti-H. pylori plasma prolonged the FMLP-induced response.
Conclusions:
- H. pylori synthesizes and secretes a substance, likely FMLP, contributing to PMNL recruitment in gastric infections.
- Immune complexes of H. pylori antigens and specific antibodies potentiate the PMNL oxidative burst.
- The interplay between H. pylori products, host PMNLs, and antibodies may drive mucosal damage in H. pylori-associated gastritis.
Related Concept Videos
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
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 to M3...
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 to M3...
01:16Treating 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...
01:28Peptic 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.
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.
01:27Peptic 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...
01:26Gastritis 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...
01:24Peptic 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...