Neutrophil-derived heparin binding protein-A mediator of increased vascular permeability after burns?

被引:20
作者
Johansson, Joakim [1 ]
Lindbom, Lennart [2 ]
Herwald, Heiko [3 ]
Sjoberg, Folke
机构
[1] Linkoping Univ Hosp, Div Perioperat Med, Dept Perioperat Med, Fac Hlth Sci, S-58185 Linkoping, Sweden
[2] Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden
[3] Lund Univ, Dept Clin Sci, Div Infect Med, Lund, Sweden
关键词
Azurocidin; Burn; CAP-37; HBP; Trauma; Vascular permeability; INFLAMMATORY MEDIATOR; THERMAL-INJURY; SECRETION; HBP/CAP37; RECEPTORS; MONOCYTES; ADHESION; CAP37;
D O I
10.1016/j.burns.2009.02.021
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Increased vascular permeability and oedema formation constitute a major clinical challenge following burns. Several clinical studies show that leukocytes are systemically activated following burns. Neutrophils have the capability to increase vascular permeability via mechanisms thought to involve the release of heparin binding protein (HBP). We hypothesised that HBP is elevated in plasma after major burns due to a systemic inflammatory response and investigated plasma-HBP concentrations in 10 severely burned patients daily for 1 week following the burn. Five-fold higher levels in plasma-HBP concentration compared to a control group were detected on the first day after injury, followed by a steep reduction in the time-period that corresponds to the last part of the hyperpermeability phase. These data are in accordance with the hypothesis that HBP may function as a mediator of the early bum-induced increase in vascular permeability, and call for further studies to confirm a possible cause-and-effect relationship between HBP and oedema formation following burns. (C) 2009 Elsevier Ltd and ISBI. All rights reserved.
引用
收藏
页码:1185 / 1187
页数:3
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