Interleukin 10, monocytes and increased risk of early infection in ischaemic stroke. Issue 11 (16th October 2006)

• Record Type: Journal Article
• Authors: Chamorro, Á; Amaro, S; Vargas, M; Obach, V; Cervera, Á; Torres, F; Planas, A M
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 77:Issue 11(2006)
• Page Start: 1279
• Page End: 1281
• Publication Date: 2006-10-16
• Subjects: IFN, interferon -- SAI, stroke-associated infection -- TNF, tumour necrosis factor; Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp.2006.100800
• Languages: English
• ISSNs: 0022-3050

Abstract

Abstract : 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)α 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 TNFα and the TNFα/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.