4.2 Article

Serum and cerebrospinal fluid levels of cytokines in acute encephalopathy associated with human herpesvirus-6 infection

期刊

BRAIN & DEVELOPMENT
卷 31, 期 10, 页码 731-738

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.braindev.2008.11.005

关键词

Cytokine; Encephalopathy; Human herpesvirus-6; Interleukin-6; Soluble tumor necrosis factor receptor

资金

  1. Ministry of Health, Labour, and Welfare [H18-Shinkou-6]
  2. Ministry of Education, Culture, Sports, Science and Technology, Japan [A-17209037]

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Human herpesvirus-6 (HHV-6) is a causative agent of exanthema subitum. The immunological pathogenesis of acute encephalopathy associated with HHV-6 infection is still unclear. We measured the concentrations of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-2 (IL-2), IL-4 IL-6, IL-10, and soluble TNF receptor 1 (sTNFR1)in serum and cerebrospinal fluid (CSF) during the acute stage in 15 infants with acute encephalopathy and 12 with febrile seizures associated with HHV-6 infection. The serum IL-6. IL-10, sTNFR1, CSF IL-6, and sTNFR1 levels of infants with encephalopathy who had neurological sequelae (n = 9) were significantly higher than those with febrile seizures (p = 0.011, 0.043 0.002, 0.029, and 0.005, respectively). In acute encephalopathy, serum IL-6, sTNFR1, and CSF IL-6 levels in infants with neurological sequelae were significantly higher than those without (n = 6) neurological sequelae (p = 0.043 0.026, and 0.029, respectively), and serum IFN-gamma, IL-6, IL-10, and sTNFR1 levels were significantly higher than those in the CSF (p = 0.037 0.037, 0.001, and 0.021, respectively). There were no significant differences in serum or CSF cytokine levels between infants who were positive For HHV-6 DNA in the CSF (17 = 6) compared to those who were negative (n = 9). We Suggest that cytokines mediate the pathogenesis of acute encephalopathy associated with HHV-6 infection, and that the elevated levels of serum IL-6, sTNFR1, and CSF IL-6 are important for predicting neurological sequelae. (C) 2008 Elsevier B.V. All rights reserved.

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