Opening the flood-gates: how neutrophil-endothelial interactions regulate permeability.

Abstract:

:Many diseases have an inflammatory component, where neutrophil interactions with the vascular endothelium lead to barrier dysfunction and increased permeability. Neutrophils increase permeability through secreted products such as the chemokines CXCL1, 2, 3, and 8, through adhesion-dependent processes involving beta(2) integrins interacting with endothelial ICAM-1, and through combinations where beta(2) integrin engagement leads to degranulation and secretion of heparin-binding protein. Some neutrophil products, such as arachidonic acid or the leukotriene LTA4, are further processed by endothelial enzymes via transcellular metabolism before the resulting products thromboxane A2 or LTC4 can activate their cognate receptors. Neutrophils also generate reactive oxygen species that induce vascular leakage. This review focuses on the mechanisms of neutrophil-mediated leakage.

journal_name

Trends Immunol

journal_title

Trends in immunology

authors

DiStasi MR,Ley K

doi

10.1016/j.it.2009.07.012

subject

Has Abstract

pub_date

2009-11-01 00:00:00

pages

547-56

issue

11

eissn

1471-4906

issn

1471-4981

pii

S1471-4906(09)00157-4

journal_volume

30

pub_type

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