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Updated: Jul 29, 2026
One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
Published on: June 18, 2016
Additive effects of Helicobacter pylori lipopolysaccharide and proteins in monocyte inflammatory responses
P S Hansen1, S B Petersen, K Varning
1Dept of Clinical Immunology, Aalborg Hospital, and Institute of Biotechnology, Aalborg University, Denmark. syrak@dadlnet.dk
Background:
Chronic active gastritis associated with Helicobacter pylori infection is characterized by both a neutrophil and a mononuclear leukocyte infiltrate. While neutrophil functions in relation to H. pylori are well described, the interactions between Helicobacter bacterial factors and monocytes are poorly understood in relation to the mucosal inflammatory process.
Methods:
Sonicates of a clinical strain as well as of a type strain of H. pylori were prepared in vitro. Monocytes from healthy donors were induced to release L-selectin (CD62L), to upregulate the adherence molecules (CD11a, CD11b. CD11c) and to produce toxic oxygen radicals. The inducing activities were assessed by flow cytometry and chemiluminescence.
Results:
A dose-dependent shedding of CD62L and upregulation of CD11b and CD11c were observed with both bacterial strains as well as PMA and fMLP. CD11a remained unchanged. Activity could be attributed to bacterial factors of both lipopolysaccharide (LPS) and protein characteristics. The alterations observed for CD11b, CD11c and CD62L were induced by the same protein fractions in parallel. suggesting a common component and mechanism of action. A major protein component was urease, although other minor protein bands were found as well. Monoclonal antibodies to CD14-inhibited monocyte inflammatory responses induced by H. pylori sonicate at low concentration, whereas further LPS pierce-matrix reduction was necessary at high sonicate concentrations to reduce monocyte-inducing activity.
Conclusions:
Monocyte inflammatory activation is induced by H. pylori sonicate components. Factors of both LPS and protein characteristics are involved and an additive effect was demonstrated. Urease appears to be a major component in the protein preparations of highest inducing capacity. Further studies are warranted to assess whether the monocyte activation properties described here are related to the diversity of clinical gastroduodenal outcome for the chronic type B gastritis associated with H. pylori infection.
Insights
Helicobacter pylori infection activates monocytes via bacterial components like LPS and urease, contributing to gastritis. Understanding these interactions is key to diverse clinical outcomes in H. pylori-associated gastritis.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Chronic active gastritis involves neutrophils and mononuclear leukocytes.
- Helicobacter pylori interactions with monocytes in gastritis are poorly understood.
Purpose of the Study:
- Investigate Helicobacter pylori components that activate human monocytes.
- Determine the role of bacterial factors in monocyte inflammatory responses.
Main Methods:
- Prepared H. pylori sonicates from clinical and type strains.
- Induced monocyte activation (CD62L release, adherence molecule upregulation, oxygen radical production).
- Assessed monocyte responses using flow cytometry and chemiluminescence.
Main Results:
- H. pylori sonicates dose-dependently altered monocyte CD62L, CD11b, and CD11c expression.
- Both lipopolysaccharide (LPS) and protein components induced these changes.
- Urease was identified as a major protein component responsible for monocyte activation.
Conclusions:
- H. pylori components, including LPS and urease, induce monocyte inflammatory activation.
- These findings suggest a mechanism contributing to H. pylori-associated gastritis.
- Further research is needed to link these monocyte responses to clinical outcomes.
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