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How neutrophils resist shear stress at blood vessel walls: molecular mechanisms, subcellular structures, and cell-cell interactions.

Abstract：

:Neutrophils are the first cells arriving at sites of tissue injury or infection to combat invading pathogens. Successful neutrophil recruitment to sites of inflammation highly depends on specific molecular mechanisms, fine-tuning the received information into signaling pathways and converting them into well-described recruitment steps. This review highlights the impact of vascular flow conditions on neutrophil recruitment and the multitude of mechanisms developed to enable this sophisticated process under wall shear stress conditions. The recruitment process underlies a complex interplay between adhesion and signaling molecules, as well as chemokines, in which neutrophils developed specific mechanisms to travel to sites of lesion in low and high shear stress conditions. Rolling, as the first step in the recruitment process, highly depends on endothelial selectins and their ligands on neutrophils, inducting of intracellular signaling and subsequently activating β2 integrins, enabling adhesion and postadhesion events. In addition, subcellular structures, such as microvilli, tethers, and slings allow the cell to arrest, even under high wall shear stress. Thereby, microvilli that are pulled out from the cell body form tethers that develop into slings upon their detachment from the substrate. In addition to the above-described primary capture, secondary capture of neutrophils via neutrophil-neutrophil or neutrophil-platelet interaction promotes the process of neutrophil recruitment to sites of lesion. Thus, precise mechanisms based on a complex molecular interplay, subcellular structures, and cell-cell interactions turn the delicate process of neutrophil trafficking during flow into a robust response allowing effective neutrophil accumulation at sites of injury.

journal_name

J Leukoc Biol

journal_title

Journal of leukocyte biology

authors

Begandt D,Thome S,Sperandio M,Walzog B

doi

10.1189/jlb.3MR0117-026RR

subject

Has Abstract

pub_date

2017-09-01 00:00:00

pages

699-709

issue

eissn

0741-5400

issn

1938-3673

pii

jlb.3MR0117-026RR

journal_volume

102

pub_type

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How neutrophils resist shear stress at blood vessel walls: molecular mechanisms, subcellular structures, and cell-cell interactions.