Neutrophil degranulation by Helicobacter pylori proteins
A Nøorgaard1, L P Andersen, H Nielsen
1Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.
Gut
|March 1, 1995
Summary
Helicobacter pylori proteins directly stimulate neutrophils, causing the release of myeloperoxidase. This bacterial stimulation contributes to increased mucosal myeloperoxidase in H. pylori-associated gastric diseases.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Helicobacter pylori infection is associated with increased myeloperoxidase in gastric mucosa.
- Neutrophils play a key role in the inflammatory response to H. pylori.
Purpose of the Study:
- To investigate the interaction between H. pylori sonicate proteins and neutrophils.
- To determine the mechanism of myeloperoxidase release and neutrophil priming by H. pylori.
Main Methods:
- Neutrophil degranulation and myeloperoxidase release were assessed using direct stimulation assays.
- H. pylori sonicate (crude and modified) was used to prime neutrophils before stimulation with fMLP or opsonized zymosan (OZ).
- Modifications included heat treatment, pronase inactivation, and dialysis to identify the active components.
Main Results:
- H. pylori sonicate proteins directly stimulated neutrophil degranulation and myeloperoxidase release in a concentration-dependent manner.
- H. pylori sonicate exhibited priming activity, enhancing neutrophil responses to subsequent stimuli like fMLP and OZ.
- While protein components were implicated, non-protein molecules like lipopolysaccharides also contributed to the priming activity.
Conclusions:
- H. pylori directly stimulates inflammatory neutrophils, leading to myeloperoxidase release.
- Bacterial-derived components from H. pylori contribute to neutrophil activation and inflammation in the gastric mucosa.
- This interaction may explain the elevated mucosal myeloperoxidase observed in H. pylori-associated diseases.
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