• Pat Tanzi, Kevin Cain, Angela Kalil, Dannielle Zierath, Anna Savos, J Michael Gee, Dean Shibata, Jessica Hadwin, Kelly Carter, and Kyra Becker.
• Department of Neurology, University of Washington, School of Medicine, Harborview Medical Center, Box 359775, 325 9th Ave, Seattle, WA 98104-2499, USA.
• Neurocrit Care. 2011 Apr 1;14(2):244-52.

BackgroundInfection is common following stroke and is independently associated with worse outcome. Clinical studies suggest that infections occur more frequently in those individuals with stroke-induced immunologic dysfunction. This study sought to explore the contribution of immunomodulatory cytokines and hormones to lymphocyte function and infection risk.MethodsPatients (N = 112) were enrolled as soon as possible after the onset of ischemic stroke. Blood was drawn to assess plasma cortisol, IL-10, IL-1ra, lymphocyte numbers, and lymphocyte function at 72 h after stroke onset; infections were censored through 21 days after stroke onset.ResultsInfection occurred in 25% of patients. Stroke severity was the most important predictor of infection risk. Increased plasma cortisol, IL-10, and IL-1ra, as well as decreased lymphocyte numbers, at 72 h after stroke onset were associated with risk of subsequent infection. After controlling for stroke severity, only IL-1ra was independently associated with infection risk, and the degree of risk was consistent throughout the post-stroke period. Infection, but not IL-1ra itself, was associated with worse outcome at 3 months.ConclusionsIn this study cohort, increased plasma IL-1ra was independently associated with the risk of post-stroke infection. Further studies are needed to validate this finding, which could have important implications for stroke therapy.

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