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Helicobacter pylori...
Helicobacter pylori induce neutrophil transendothelial migration: role of the bacterial HP-NAP
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- Brisslert, Mikael, 1974 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
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- Enarsson, Karin, 1975 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology
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- Lundin, Samuel B, 1970 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology
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- Karlsson, Anna, 1967 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
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Kusters, J. G. (author)
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- Svennerholm, Ann-Mari, 1947 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology
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Backert, S. (author)
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- Quiding-Järbrink, Marianne, 1964 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology
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(creator_code:org_t)
- 2005
- 2005
- English.
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In: FEMS Microbiol Lett. ; 249:1, s. 95-103
- Related links:
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Abstract
Subject headings
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- Continuous recruitment of neutrophils into the inflamed gastric mucosal tissue is a hallmark of Helicobacter pylori infection in humans. In this study, we examined the ability of H. pylori to induce transendothelial migration of neutrophils using a transwell system consisting of a cultured monolayer of human endothelial cells as barrier between two chambers. We showed for the first time that live H. pylori, but not formalin-killed bacteria, induced a significantly increased transendothelial migration of neutrophils. H. pylori conditioned culture medium also induced significantly increased transendothelial migration, whereas heat-inactivated culture filtrates had no effect, suggesting that the chemotactic factor was proteinaceous. Depletion of H. pylori-neutrophil activating protein (HP-NAP) from the culture filtrates resulted in significant reduction of the transmigration. Culture filtrates from isogenic HP-NAP deficient mutant bacteria also induced significantly less neutrophil migration than culture filtrates obtained from wild-type bacteria. HP-NAP did not induce endothelial cell activation, suggesting that HP-NAP acts directly on the neutrophils. In conclusion, our results demonstrate that secreted HP-NAP is one of the factors resulting in H. pylori induced neutrophil transendothelial migration. We propose that HP-NAP contributes to the continuous recruitment of neutrophils to the gastric mucosa of H. pylori infected individuals.
Keyword
- Bacterial Proteins/genetics/*metabolism/pharmacology
- Cells
- Cultured
- Chemotactic Factors/genetics/metabolism/pharmacology
- Chemotaxis
- Leukocyte/*drug effects
- Endothelial Cells/*immunology
- Endothelium
- Vascular/cytology/immunology
- Helicobacter pylori/genetics/*immunology/metabolism
- Humans
- Neutrophil Activation/immunology
- Neutrophils/*immunology
- Research Support
- Non-U.S. Gov't
Publication and Content Type
- ref (subject category)
- art (subject category)
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