Sympathetic activation triggers systemic interleukin-10 release in immunodepression induced by brain injury

被引：346
作者：
Woiciechowsky, C
Asadullah, K
Nestler, D
Eberhardt, B
Platzer, C
Schöning, B
Glöckner, F
Lanksch, WR
Volk, HD
Döcke, WD
机构：
[1] Humboldt Univ, Med Sch Charite, Dept Med Immunol, D-10098 Berlin, Germany
[2] Humboldt Univ, Med Sch Charite, Dept Dermatol, D-10098 Berlin, Germany
[3] Humboldt Univ, Med Sch Charite, Dept Neurosurg, D-10098 Berlin, Germany
[4] Univ Jena, Sch Med, Inst Anat 2, D-07740 Jena, Germany
来源：
NATURE MEDICINE | 1998年 / 4卷 / 07期
关键词：
D O I：
10.1038/nm0798-808
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The mechanism of immunodepression after brain injury is not yet clear. Here we demonstrate rapid systemic release of the immunoinhibitory cytokine interleukin-10, monocytic deactivation and a high incidence of infection in patients with 'sympathetic storm' due to acute accidental or iatrogenic brain trauma. In vitro studies showed that within minutes catecholamines trigger the secretion of interleukin-10 from unstimulated monocytes through a beta-adrenoreceptor-mediated, cAMP/protein kinase A-dependent pathway. We found that in a rat model of acute brain injury, the beta-receptor antagonist propranolol prevented the increase of interleukin-10 plasma levels. Rapid monocytic interleukin-10 release after sympathetic activation may represent a common pathway for immunodepression induced by stress and injury.
引用
收藏
页码：808 / 813
页数：6
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