INHIBITION OF ENDOTOXIN-INDUCED CYTOKINE RELEASE AND NEUTROPHIL ACTIVATION IN HUMANS BY USE OF RECOMBINANT BACTERICIDAL PERMEABILITY-INCREASING PROTEIN

被引：103

作者：

VONDERMOHLEN, MAM

KIMMINGS, AN

WEDEL, NI

MEVISSEN, MLCM

JANSEN, J

FRIEDMANN, N

LORENZ, TJ

NELSON, BJ

WHITE, ML

BAUER, R

HACK, CE

EERENBERG, AJM

VANDEVENTER, SJH

机构：

[1] NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,AMSTERDAM,NETHERLANDS

[2] XOMA CORP,BERKELEY,CA 94710

来源：

JOURNAL OF INFECTIOUS DISEASES | 1995年 / 172卷 / 01期

关键词：

D O I：

10.1093/infdis/172.1.144

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 investigate the effects of a recombinant endotoxin-binding protein, bactericidal/permeability-increasing protein (rBPI(23)), on cytokine release and neutrophil activation in endotoxemia in humans, 8 volunteers were challenged twice with endotoxin and concurrently received either rBPI(23) or placebo in a randomized, placebo controlled, double-blind crossover study. rBPI(23) treatment significantly lowered circulating endotoxin levels (P = .02) and resulted in a significant reduction in the release of tumor necrosis factor (TNF), soluble TNF receptors p55 and p75, interleukin (IL)-6, IL-8 (P < .01 for each), and IL-10 levels (P = .02) but did not prevent the endotoxin-induced rise in body temperature. The early endotoxin-induced leukopenia was blunted (P = .08), and neutrophil degranulation, as measured by circulating levels of elastase/alpha(1)-antitrypsin complexes (P = .03) and lactoferrin (P < .01), was largely prevented by rBPI(23). The results of this study indicate that rBPI(23) is capable of neutralizing many of the biologic effects of endotoxin in humans.

引用

页码：144 / 151

页数：8

共 51 条

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