Tumor necrosis factor receptor-associated death domain mediated neuronal death contributes to the glial activation and subsequent neuroinflammation in Japanese encephalitis

Vivek Swarup, Joydeep Ghosh, Sulagna Das, Anirban Basu

Research output: Contribution to journalArticle

44 Scopus citations

Abstract

While a number of studies have documented the importance of microglia in central nervous system (CNS) response to injury, infection and in disease state, little is known regarding how the neuronal death initiates the cascades of secondary neuroinflammation. We have exploited an experimental model of Japanese encephalitis to better understand how neuronal death following viral infection initiates microglial activation following Japanese encephalitis virus infection. We have earlier shown that the altered expression of tumor necrosis factor receptor-1 (TNFR-1) and TNFR associated death domain (TRADD) following Japanese encephalitis virus infection regulates the downstream apoptotic cascades. Here we have reported that silencing TRADD expression with small-interfering RNA reduced neuronal apoptosis and subsequent microglial and astroglial activation and release of various pro-inflammatory mediators. Our findings suggest that the engagement of TNFR-1 and TRADD following Japanese encephalitis virus infection plays a crucial role in glial activation also and influences the outcome of viral pathogenesis.

Original languageEnglish (US)
Pages (from-to)1310-1321
Number of pages12
JournalNeurochemistry International
Volume52
Issue number7
DOIs
StatePublished - Jun 1 2008
Externally publishedYes

Keywords

  • Astrocytes
  • Cell adhesion molecule
  • Chemokine receptor
  • Iba-1
  • Japanese Encephalitis Virus
  • Microglia
  • Proinflammatory cytokines
  • TRADD
  • VEGF

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

Fingerprint Dive into the research topics of 'Tumor necrosis factor receptor-associated death domain mediated neuronal death contributes to the glial activation and subsequent neuroinflammation in Japanese encephalitis'. Together they form a unique fingerprint.

  • Cite this