Abstract

Objectives: Japanese encephalitis (JE) is one of the commonest viral encephalitis especially prevalent in Southeast Asia. Estimated mortality rate of JE is ∼30%, with survivors undergoing severe and irreversible neurological sequelae. Although central nervous system (CNS) inflammation is imminent upon JE infection, the pathways underlying the same have not yet been clearly elucidated. However, cytokines–tumor necrosis factor-α (TNF-α) and interlukin-2 (IL-2), are small secreted proteins, which mediate and regulate immunity. Therefore, we wanted to evaluate the role, if any, of these cytokines in the pathogenesis of JE.Methods: We measured the levels of TNF-α and IL-2 in the serum and cerebrospinal fluid (CSF) of patients suffering JE, using enzyme-linked immunosorbent assay (ELISA).Results: JE infection caused a remarkable increase (p<0.0001) in the levels of TNF-α in the serum and CSF, while IL-2 levels were unaffected.Discussion: These results show that TNF-α pathway is involved in JE infection-triggered neuroinflammation.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call