Kenji Yone

Tumor necrosis factor and interleukin-1 in the CSF and sera of patients with multiple sclerosis

Serum and cerebrospinal fluid (CSF) from 31 patients with multiple sclerosis (MS) were examined to determine the levels of tumor necrosis factor (TNF) and interleukin (IL)-1 alpha (or IL-1 beta) by an enzyme-linked immunosorbent assay. TNF was detected in 29 (93.5%) of CSF from 31 cases of MS. TNF was also detectable in 100% of CSF from patients with acute relapsing MS in exacerbation. Patients with acute relapsing MS in exacerbation showed significantly higher CSF levels of TNF as compared with either those in remission or the controls (P less than 0.001 and P less than 0.0001, respectively). Increased levels of TNF were also detected in 35.5% of the MS sera, and especially in those with acute relapsing MS in exacerbation. Increased TNF levels were also frequent in the CSF and sera of patients with Guillain-Barré syndrome (GBS), which is also a demyelinating disease. No IL-1 alpha (or IL-1 beta) was detected in either CSF or sera of 31 MS patients. It is considered likely that TNF CSF levels may reflect disease activity in MS.

Tumor necrosis factor-α inhibitory activity in urine of Kawasaki disease☆

Abstract Recently it has been reported that naturally occurring inhibitors of tumor necrosis factor α (TNF-α) were demonstrated in urine of some acute febrile patients. We investigated whether TNF-α inhibitory activity in urine increases during acute Kawasaki disease (KD). TNF-α inhibitory activities in urine were measured by a cytotoxicity assay on the TNF-susceptible cell line L929. KD patients had increased TNF-α inhibitory activities in urine during the acute stage and returned to a normal range during the convalescent stage. Our results suggest that the TNF-α inhibitor in urine is part of the regulatory system of TNF-α, which might be responsible for vascular injury during acute KD.