BACKGROUND: Influenza virus-associated encephalopathy (IE) is suggested to be a proinflammatory cytokine-related disease. METHODS: We measured the concentrations of interleukin-6 (IL-6), TNF-alpha, soluble TNF receptor 1 (sTNFR1), IL-10, interferon-gamma, IL-2, IL-4, and soluble E-selectin (sE-selectin) in serum and CSF during the acute stage in 30 children with IE, 20 with influenza virus-associated febrile seizures (IFS), and 39 with influenza virus infection without complications (Flu). Moreover, the activation of transcription factor NF-kappaB in peripheral blood mononuclear cells (PBMC) of 5 children with IE was examined. RESULTS: The serum IL-6, sTNFR1, and IL-10 levels in the IE group with a poor prognosis (Group A) were significantly higher than those in the IE group without sequelae in IE (Group B), IFS, and Flu. In particular, the serum levels of IL-6, sTNFR1, and IL-10 in 5 deceased patients were markedly higher. The CSF IL-6 levels in Group A were significantly higher than those in Group B and IFS. Flow cytometric analysis revealed that NF-kappaB activation in PBMC in Group A was higher than that in Group B, IFS, and Flu. CONCLUSION: We suggest that cytokines are produced by PBMC in IE, and that the levels of serum IL-6, sTNFR1, and IL-10, CSF IL-6, and NF-kappaB activation in PBMC are useful indicators of the severity of the disease.
BACKGROUND:Influenza virus-associated encephalopathy (IE) is suggested to be a proinflammatory cytokine-related disease. METHODS: We measured the concentrations of interleukin-6 (IL-6), TNF-alpha, soluble TNF receptor 1 (sTNFR1), IL-10, interferon-gamma, IL-2, IL-4, and soluble E-selectin (sE-selectin) in serum and CSF during the acute stage in 30 children with IE, 20 with influenza virus-associated febrile seizures (IFS), and 39 with influenza virus infection without complications (Flu). Moreover, the activation of transcription factor NF-kappaB in peripheral blood mononuclear cells (PBMC) of 5 children with IE was examined. RESULTS: The serum IL-6, sTNFR1, and IL-10 levels in the IE group with a poor prognosis (Group A) were significantly higher than those in the IE group without sequelae in IE (Group B), IFS, and Flu. In particular, the serum levels of IL-6, sTNFR1, and IL-10 in 5 deceased patients were markedly higher. The CSF IL-6 levels in Group A were significantly higher than those in Group B and IFS. Flow cytometric analysis revealed that NF-kappaB activation in PBMC in Group A was higher than that in Group B, IFS, and Flu. CONCLUSION: We suggest that cytokines are produced by PBMC in IE, and that the levels of serum IL-6, sTNFR1, and IL-10, CSF IL-6, and NF-kappaB activation in PBMC are useful indicators of the severity of the disease.
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