title: Post-stroke infection: a role for IL-1ra?
abstract: BACKGROUND
  Infection 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.
  
  
  METHODS
  Patients (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.
  
  
  RESULTS
  Infection 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.
  
  
  CONCLUSIONS
  In 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.
authors.affiliation: Department of Neurology, University of Washington, School of Medicine, Harborview Medical Center, Box 359775, 325 9th Ave, Seattle, WA 98104-2499, USA.
authors.forename: Pat
authors.initials: P
authors.lastname: Tanzi
authors.forename: Kevin
authors.initials: K
authors.lastname: Cain
authors.forename: Angela
authors.initials: A
authors.lastname: Kalil
authors.forename: Dannielle
authors.initials: D
authors.lastname: Zierath
authors.forename: Anna
authors.initials: A
authors.lastname: Savos
authors.forename: J Michael
authors.initials: JM
authors.lastname: Gee
authors.forename: Dean
authors.initials: D
authors.lastname: Shibata
authors.forename: Jessica
authors.initials: J
authors.lastname: Hadwin
authors.forename: Kelly
authors.initials: K
authors.lastname: Carter
authors.forename: Kyra
authors.initials: K
authors.lastname: Becker
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015331:Cohort Studies; D003422:Critical Care; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000276:immunology; D007239:Infections / Q000453:epidemiology* / Q000276:immunology*; D053590:Interleukin 1 Receptor Antagonist Protein / Q000097:blood / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012720:Severity of Illness Index; D020521:Stroke / Q000453:epidemiology* / Q000276:immunology*
chemical_list: D053590:Interleukin 1 Receptor Antagonist Protein; D006854:Hydrocortisone