Blood-Brain Barrier Damage in Patients with Bacterial Meningitis: Association with Tumor Necrosis Factor-α but Not Interleukin-1β

Brain damage after meningeal infection could result from impairment of cerebral endothelial cell functions and disruption of blood-brain barriers. Tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) produce many of their effects by acting on endothelial cells. This study correlates levels of TNFα and IL-1β in paired cerebrospinal fluid (CSF) and serum samples with the degree of blood-brain barrier damage, as manifested by CSF to serum albumin quotient, in 48 patients with bacterial meningitis and 66 controls. CSF levels of TNFα and IL-1β in bacterial meningitis were significantly higher than in controls. Intrathecal levels of TNFα, but not IL-1β correlated with albumin quotient (P < .001), with degree of blood-brain barrier disruption (P < .001), and with disease severity and indices of meningeal inflammation. Sequential CSF samples demonstrated that IL-1β and TNFα disappear from the CSF within 24 h of antibiotic treatment. Data presented here suggest that TNFα is related to blood-brain barrier damage in bacterial meningitis and that its effect could be dissociated from that of IL-1β.