Interleukin 10, monocytes and increased risk of early infection in ischaemic stroke

被引:96
作者
Chamorro, A. [1 ]
Amaro, S.
Vargas, M.
Obach, V.
Cervera, A.
Torres, F.
Planas, A. M.
机构
[1] Univ Barcelona, Hosp Clin, Stroke Unit, IDIBAPS, E-08036 Barcelona, Spain
[2] CSIC, IIIB, Consejo Super Incest Cientif, Dept Pharmacol & Toxicol, Barcelona, Spain
[3] Hosp Clin Barcelona, Unitat Avaluacio Suport Proyectes, Clin Pharmacol Unit, Barcelona, Spain
关键词
MECHANISMS; COMPLICATIONS; ACTIVATION; TRIAL; BRAIN;
D O I
10.1136/jnnp.2006.100800
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and purpose: The pathophysiology of stroke-associated infection (SAI) is uncertain. The cytokine profile and peripheral white cell response were assessed in patients with or without SAI. Methods: The incidence of SAI was assessed in 110 patients with ischaemic stroke allocated antibiotic prophylaxis or placebo within 24 h of clinical onset. Peripheral white cell counts, interleukin (IL)6, tumour necrosis factor (TNF)alpha and IL10 were measured in plasma. Results: 17 (15%) patients developed infection and showed time-dependent increases of total white cell count, neutrophils, monocytes, lymphocytes, IL6 and IL10, whereas TNF alpha and the TNF alpha/IL10 ratio decreased. In logistic regression, IL10 (odds ratio (OR) 1.08, 95% confidence interval (CI) 1.01 to 1.16), monocyte count (OR 1.42, 95% CI 1.08 to 1.87) and National Institute for Health Stroke Survey score on admission (OR 1.17, 95% CI 1.05 to 1.31) were independent predictors of systemic infection. Conclusions: SAI is associated with stroke severity, excessive IL10-mediated response and an increased number of circulating monocytes. These results support the finding that acute ischaemic brain injury triggers a blood-borne anti-inflammatory response that decreases the antimicrobial drive of the immune system.
引用
收藏
页码:1279 / 1281
页数:3
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