Chemokine- and adhesion-dependent survival of neutrophils after transmigration through cytokine-stimulated endothelium

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@article{c6a779c36cd44698bccae644ef2811d3,
title = "Chemokine- and adhesion-dependent survival of neutrophils after transmigration through cytokine-stimulated endothelium",
abstract = "We examined the fate of neutrophils following transmigration through an endothelial monolayer cultured on {"}Transwell{"} membrane filters. Treatment of human umbilical vein endothelial cells (HUVEC) with increasing doses of tumor necrosis factor-alpha increased the efficiency of transmigration and markedly reduced apoptosis among the transmigrated neutrophils in a dose-dependent manner. Apoptosis was also inhibited after transmigration of neutrophils through HUVEC stimulated with interleukin (IL)-1beta but not so effectively after chemotaxis through unstimulated HUVEC driven by IL-8 added below the filter. Inhibition of beta2-integrin binding after transmigration or coating the lower chamber with a nonadhesive polymer (polyhydroxyl-ethyl-methacrylate) abrogated neutrophil survival. Although integrin engagement during migration itself was not essential to inhibit apoptosis, activation of neutrophils through CXC chemokine receptors was necessary. Quite brief exposure to the HUVEC (30-120 min) was effective in reducing subsequent apoptosis, although if coincubation with the HUVEC were prolonged, neutrophil apoptosis was reduced further. Neutralization of granulocyte macrophage-colony stimulating factor inhibited this additional effect. Thus, a complex interplay between migration- and activation-dependent signals and adhesive interaction in tissue may combine to effectively prolong the survival of neutrophils recruited during inflammation.",
keywords = "endothelial cells, apoptosis, adhesion molecules, leukocyte trafficking",
author = "Helen McGettrick and Janet Lord and Ke-Qing Wang and George Rainger and Christopher Buckley and Gerard Nash",
year = "2006",
month = jan,
day = "13",
doi = "10.1189/jlb.0605350",
language = "English",
volume = "79",
pages = "779--788",
journal = "Journal of Leukocyte Biology",
issn = "0741-5400",
publisher = "Society for Leukocyte Biology",
number = "4",

}

RIS

TY - JOUR

T1 - Chemokine- and adhesion-dependent survival of neutrophils after transmigration through cytokine-stimulated endothelium

AU - McGettrick, Helen

AU - Lord, Janet

AU - Wang, Ke-Qing

AU - Rainger, George

AU - Buckley, Christopher

AU - Nash, Gerard

PY - 2006/1/13

Y1 - 2006/1/13

N2 - We examined the fate of neutrophils following transmigration through an endothelial monolayer cultured on "Transwell" membrane filters. Treatment of human umbilical vein endothelial cells (HUVEC) with increasing doses of tumor necrosis factor-alpha increased the efficiency of transmigration and markedly reduced apoptosis among the transmigrated neutrophils in a dose-dependent manner. Apoptosis was also inhibited after transmigration of neutrophils through HUVEC stimulated with interleukin (IL)-1beta but not so effectively after chemotaxis through unstimulated HUVEC driven by IL-8 added below the filter. Inhibition of beta2-integrin binding after transmigration or coating the lower chamber with a nonadhesive polymer (polyhydroxyl-ethyl-methacrylate) abrogated neutrophil survival. Although integrin engagement during migration itself was not essential to inhibit apoptosis, activation of neutrophils through CXC chemokine receptors was necessary. Quite brief exposure to the HUVEC (30-120 min) was effective in reducing subsequent apoptosis, although if coincubation with the HUVEC were prolonged, neutrophil apoptosis was reduced further. Neutralization of granulocyte macrophage-colony stimulating factor inhibited this additional effect. Thus, a complex interplay between migration- and activation-dependent signals and adhesive interaction in tissue may combine to effectively prolong the survival of neutrophils recruited during inflammation.

AB - We examined the fate of neutrophils following transmigration through an endothelial monolayer cultured on "Transwell" membrane filters. Treatment of human umbilical vein endothelial cells (HUVEC) with increasing doses of tumor necrosis factor-alpha increased the efficiency of transmigration and markedly reduced apoptosis among the transmigrated neutrophils in a dose-dependent manner. Apoptosis was also inhibited after transmigration of neutrophils through HUVEC stimulated with interleukin (IL)-1beta but not so effectively after chemotaxis through unstimulated HUVEC driven by IL-8 added below the filter. Inhibition of beta2-integrin binding after transmigration or coating the lower chamber with a nonadhesive polymer (polyhydroxyl-ethyl-methacrylate) abrogated neutrophil survival. Although integrin engagement during migration itself was not essential to inhibit apoptosis, activation of neutrophils through CXC chemokine receptors was necessary. Quite brief exposure to the HUVEC (30-120 min) was effective in reducing subsequent apoptosis, although if coincubation with the HUVEC were prolonged, neutrophil apoptosis was reduced further. Neutralization of granulocyte macrophage-colony stimulating factor inhibited this additional effect. Thus, a complex interplay between migration- and activation-dependent signals and adhesive interaction in tissue may combine to effectively prolong the survival of neutrophils recruited during inflammation.

KW - endothelial cells

KW - apoptosis

KW - adhesion molecules

KW - leukocyte trafficking

UR - http://www.scopus.com/inward/record.url?scp=33746434568&partnerID=8YFLogxK

U2 - 10.1189/jlb.0605350

DO - 10.1189/jlb.0605350

M3 - Article

C2 - 16461737

VL - 79

SP - 779

EP - 788

JO - Journal of Leukocyte Biology

JF - Journal of Leukocyte Biology

SN - 0741-5400

IS - 4

ER -