Characterization of bacterial DNA binding to human neutrophil surface

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Bacterial DNA activates neutrophils through a CpG- and TLR9-independent mechanism. Neutrophil activation does not require DNA internalization, suggesting that it results from the interaction of bacterial DNA with a neutrophil surface receptor. The aim of this study was to characterize the interactio...

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Detalles Bibliográficos
Autores principales: Fuxman Bass, J.I., Gabelloni, M.L., Alvarez, M.E., Vermeulen, M.E., Russo, D.M., Zorreguieta, Á., Geffner, J.R., Trevani, A.S.
Formato: JOUR
Materias:
Bacterial DNA binding
Biofilm
CpG
Inflammation
Neutrophils
TLR9
bacterial DNA
chemoattractant
deoxyribonuclease
article
biotinylation
cell culture
cell isolation
cell migration
cell surface
controlled study
DNA binding
human
human cell
neutrophil
priority journal
Base Sequence
Biofilms
Cells, Cultured
DNA Primers
DNA, Bacterial
Escherichia coli
Humans
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_00236837_v88_n9_p926_FuxmanBass
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:Bacterial DNA activates neutrophils through a CpG- and TLR9-independent mechanism. Neutrophil activation does not require DNA internalization, suggesting that it results from the interaction of bacterial DNA with a neutrophil surface receptor. The aim of this study was to characterize the interaction of bacterial DNA with the neutrophil surface. Bacterial DNA binding showed saturation and was inhibited by unlabeled DNA but not by other polyanions like yeast tRNA and poly-A. Resembling the conditions under which bacterial DNA triggers neutrophil activation, binding was not modified in the presence or absence of calcium, magnesium or serum. Treatment of neutrophils with proteases not only dramatically reduced bacterial DNA binding but also inhibited neutrophil activation induced by bacterial DNA. Experiments performed with DNA samples of different lengths obtained after digestion of bacterial DNA with DNase showed that only DNA fragments greater than ≈170-180 nucleotides competed bacterial DNA binding and retained the ability to trigger cell activation. Treatment of neutrophils with chemoattractants or conventional agonists significantly increased bacterial DNA binding. Moreover, neutrophils that underwent transmigration through human endothelial cell monolayers even in the absence of chemoattractants, exhibited higher binding levels of bacterial DNA. Together, our findings provide evidence that binding of bacterial DNA to neutrophils is a receptor-mediated process that conditions the ability of DNA to trigger cell activation. We speculate that neutrophil recognition of bacterial DNA might be modulated by the balance of agonists present at inflammatory foci. This effect might be relevant in bacterial infections with a biofilm etiology, in which extracellular DNA could function as a potent neutrophil agonist. © 2008 USCAP, Inc All rights reserved.

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