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Proinflammatory activation of neutrophils and monocytes by Helicobacter pylori is not associated with cag A, vac A or pic B genotypes
Author(s) -
Hansen Per Syrak,
Go Mae F.,
Varming Kim,
Andersen Leif P.,
Graham David Y.,
Nielsen Henrik
Publication year - 1999
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1999.tb01517.x
Subject(s) - phagocyte , respiratory burst , helicobacter pylori , monocyte , microbiology and biotechnology , proinflammatory cytokine , flow cytometry , integrin alpha m , chemiluminescence , virulence , biology , downregulation and upregulation , inflammation , chemistry , gene , immunology , phagocytosis , biochemistry , genetics , organic chemistry
Chronic Helicobacter pylori infection is associated with mucosal inflammation. The aim of the present study was to assess human neutrophil and monocyte activation induced by H pylori strains with different virulence genotypes. Bacterial sonicates from 12 strains were used to induce phagocyte up‐regulation of adherence molecule CD11b, assessed by fluorescence flow cytometry, and oxidative burst responses, assessed by chemiluminescence. A dose‐dependent induction of the expression of CD11b was observed with sonicate from all H. pylori strains on both neutrophils and monocytes. Strains negative for cag A and pic B genes had the same inducing activity of upregulation of CD11b as strains positive for these genes. A vac A‐S2 type strain had the same activity as vac A‐S1 type strains. The induction of toxic oxygen radicals by H. pylori‐activated neutrophils gave higher median values for the cag A‐positive strains than for the cag A‐negative strains. For the monocyte chemiluminescence response, cag A‐negative strains gave higher median values compared to cag A‐positive strains. We conclude that upregulation of the neutrophil and monocyte adherence molecule CDllb induced by H. pylori sonicates is not associated with the presence of cag A, pic B or mosaic pattern of vac A, and that cag A, pic B‐negative strains and vac A‐S2 strains retain their inflammatory capacity.