Influence of bacterial endotoxin on radiation-induced activation of human endothelial cells in vitro and in vivo - Interleukin-10 protects against transendothelial migration

被引:19
作者
Lindner, H
Holler, E
Gerbitz, A
Johnson, JP
Bornkamm, GW
Eissner, G
机构
[1] UNIV MUNICH,GSF,INST CLIN MOL BIOL,D-81377 MUNICH,GERMANY
[2] UNIV MUNICH,GSF,INST RADIAT BIOL,D-81377 MUNICH,GERMANY
[3] UNIV MUNICH,GSF,INST CLIN HEMATOL,D-81377 MUNICH,GERMANY
[4] UNIV MUNICH,INST IMMUNOL,D-81377 MUNICH,GERMANY
[5] UNIV MUNICH,KLINIKUM GROSSHADERN,MED CLIN 3,D-81377 MUNICH,GERMANY
关键词
D O I
10.1097/00007890-199711150-00023
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
To extend previous studies on the anti-inflammatory role of interleukin (IL)-10 in vivo, mice pretreated with IL-10 were subjected to ionizing radiation (IR), lipopolysaccharide (LPS), or both and assessed for the expression of the intercellular adhesion molecule 1 (ICAM-1) in immunohistochemical analyses, IL-10 was able to almost fully protect LPS+IR-treated animals against ICAM-1 up-regulation, Because LPS and IR also increased adhesion of peripheral blood mononuclear cells, transendothelial migration assays were performed to investigate the functional significance of these findings, IR was found to induce transendothelial migration, and this effect could be enhanced by cotreatment with LPS, in the same fashion as peripheral blood mononuclear cell adhesion, Also in this system, IL-10 proved to act as a potent LPS antagonist, Finally, in vivo immunohistochemical analyses revealed an infiltration of CD3(+) T lymphocytes into organs that were the target of transplant-related complications after LPS+IR treatment, This infiltration could also be completely reversed by IL-10 pretreatment.
引用
收藏
页码:1370 / 1373
页数:4
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