Stroke-induced immunodeficiency promotes spontaneous bacterial infections and is mediated by sympathetic activation reversal by poststroke T helper cell type 1-like immunostimulation.
Stroke-induced immunodeficiency promotes spontaneous bacterial infections and is mediated by sympathetic activation reversal by poststroke T helper cell type 1-like immunostimulation.
复制标题
DOI：
10.1084/jem.20021098
复制
发表时间：
2003-09-01
期刊：
影响因子：
--
通讯作者：
Meisel A
中科院分区：
文献类型：
--
作者：
Prass K;Meisel C;Höflich C;Braun J;Halle E;Wolf T;Ruscher K;Victorov IV;Priller J;Dirnagl U;Volk HD;Meisel A
感染是中风患者死亡的主要原因。在小鼠局灶性脑缺血模型中，我们检验了中风诱导的免疫缺陷增加细菌感染易感性的假设。缺血后3d，所有动物均出现自发性败血症和肺炎。中风引起广泛的淋巴细胞凋亡损失和从T辅助细胞（Th）1向Th 2细胞因子产生的转变。从野生型小鼠连续转移T细胞和自然杀伤细胞，而不是从干扰素（IFN）-γ缺陷小鼠，或在中风后第1天给予IFN-γ，大大降低了细菌负荷。重要的是，通过阻断交感神经系统而不是下丘脑-垂体-肾上腺轴，可以预防IFN-γ反应缺陷和细菌感染的发生。此外，给予β-肾上腺素受体阻滞剂普萘洛尔显著降低了卒中后的死亡率。这些数据表明，儿茶酚胺介导的早期淋巴细胞活化缺陷是中风后抗菌免疫反应受损的关键因素。
Infections are a leading cause of death in stroke patients. In a mouse model of focal cerebral ischemia, we tested the hypothesis that a stroke-induced immunodeficiency increases the susceptibility to bacterial infections. 3 d after ischemia, all animals developed spontaneous septicemia and pneumonia. Stroke induced an extensive apoptotic loss of lymphocytes and a shift from T helper cell (Th)1 to Th2 cytokine production. Adoptive transfer of T and natural killer cells from wild-type mice, but not from interferon (IFN)-γ–deficient mice, or administration of IFN-γ at day 1 after stroke greatly decreased the bacterial burden. Importantly, the defective IFN-γ response and the occurrence of bacterial infections were prevented by blocking the sympathetic nervous system but not the hypothalamo-pituitary-adrenal axis. Furthermore, administration of the β-adrenoreceptor blocker propranolol drastically reduced mortality after stroke. These data suggest that a catecholamine-mediated defect in early lymphocyte activation is the key factor in the impaired antibacterial immune response after stroke.
登录
查看更多内容
影响因子：
8.3
作者：
Davenport, RJ;Dennis, MS;Warlow, CP
通讯作者：
Warlow, CP
DOI：
10.1073/pnas.96.25.14541
发表时间：
1999-12-07
影响因子：
11.1
作者：
Hotchkiss, RS;Tinsley, KW;Karl, IE
通讯作者：
Karl, IE
影响因子：
5
作者：
CRUSE, JM;LEWIS, RE;BRITT, R
通讯作者：
BRITT, R
DOI：
10.1164/ajrccm/146.2.290
发表时间：
1992-08-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
HSIEH, AHH;BISHOP, MJ;PIERSON, DJ
通讯作者：
PIERSON, DJ
影响因子：
8.3
作者：
HENON, H;GODEFROY, O;PRUVO, JP
通讯作者：
PRUVO, JP