UNLABELLED: We determined the concentrations of interleukin-1beta (IL-1beta, IL-6, IL-10, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha), and soluble TNF receptor 1 (sTNFR1) in CSF from 18 patients with acute disseminated encephalomyelitis (ADEM) to investigate the role of cytokines in the pathogenesis of the disease in the acute stage. Cytokines and sTNFR1 were measured by ELISA. The CSF IL-6, IL-10, TNF-alpha, and sTNFR1 concentrations were elevated in 16, 13, 3, and 11 of the 18 patients with ADEM, respectively. CSF concentrations of IL-10 and sTNFRI correlated positively with each other in the patients (P<0.01). Myelin basic protein levels in CSF of the patients with elevated CSF sTNFR1 levels were significantly higher than those in CSF of the patients with normal CSF sTNFR1 levels (P<0.05). IL-1beta and IFN-gamma were not elevated in CSF. Our results suggest that IL-6 and TNF-alpha mediate inflammation in the central nervous systems in ADEM. We speculated that TNF-alpha is related to demyelination and that IL-10 is induced to modulate TNF-alpha-induced inflammation in ADEM. CONCLUSION: these findings suggest that cytokines such as tumour necrosis factor-alpha, soluble tumour necrosis factor receptor 1, interleukin-6, and interleukin-10 are related to the pathogenesis of acute disseminated encephalomyelitis in the acute stage.
UNLABELLED: We determined the concentrations of interleukin-1beta (IL-1beta, IL-6, IL-10, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha), and soluble TNF receptor 1 (sTNFR1) in CSF from 18 patients with acute disseminated encephalomyelitis (ADEM) to investigate the role of cytokines in the pathogenesis of the disease in the acute stage. Cytokines and sTNFR1 were measured by ELISA. The CSF IL-6, IL-10, TNF-alpha, and sTNFR1 concentrations were elevated in 16, 13, 3, and 11 of the 18 patients with ADEM, respectively. CSF concentrations of IL-10 and sTNFRI correlated positively with each other in the patients (P<0.01). Myelin basic protein levels in CSF of the patients with elevated CSF sTNFR1 levels were significantly higher than those in CSF of the patients with normal CSF sTNFR1 levels (P<0.05). IL-1beta and IFN-gamma were not elevated in CSF. Our results suggest that IL-6 and TNF-alpha mediate inflammation in the central nervous systems in ADEM. We speculated that TNF-alpha is related to demyelination and that IL-10 is induced to modulate TNF-alpha-induced inflammation in ADEM. CONCLUSION: these findings suggest that cytokines such as tumour necrosis factor-alpha, soluble tumour necrosis factor receptor 1, interleukin-6, and interleukin-10 are related to the pathogenesis of acute disseminated encephalomyelitis in the acute stage.