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Helicobacter pylori induce neutrophil transendothelial migration: role of the bacterial HP-NAP

Journal article
Authors Mikael Brisslert
Karin Enarsson
Samuel B Lundin
Anna Karlsson
J. G. Kusters
Ann-Mari Svennerholm
S. Backert
Marianne Quiding-Järbrink
Published in FEMS Microbiol Lett
Volume 249
Issue 1
Pages 95-103
Publication year 2005
Published at Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
Institute of Medical Microbiology/Immunology
Pages 95-103
Language en
Keywords 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
Subject categories Medical and Health Sciences


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.

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