Infectious bursal disease virus infection induces macrophage activation via p38 MAPK and NF-κB pathways

Mahesh Khatri, Jagdev M. Sharma

Research output: Contribution to journalArticlepeer-review

61 Scopus citations


In the present study, we show that infection with infectious bursal disease virus (IBDV) causes activation of macrophages, the key cells involved in inflammatory and immune-regulatory functions. Exposure of cultured spleen macrophages (SM) from SPF chickens to IBDV resulted in the production of nitric oxide (NO). In addition, there was upregulation of mRNA expression of inducible nitric oxide synthase (iNOS), IL-8 and cyclooxygenase-2 (COX-2). The signal transduction pathways involved in macrophage activation were examined. The role of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) was tested by using specific pharmacological inhibitors. Addition of p38 MAPK inhibitor, SB-203580 and NF-κB inhibitor Bay 11-7082, suppressed IBDV-induced NO production and mRNA expression of iNOS, IL-8 and COX-2. The results suggest that IBDV uses cellular signal transduction machinery, in particular the p38 MAPK and NF-κB pathways, to elicit macrophage activation. The increased production of NO, IL-8 and COX-2 by macrophages may contribute to bursa inflammatory responses commonly seen during the acute IBDV infection.

Original languageEnglish (US)
Pages (from-to)70-77
Number of pages8
JournalVirus research
Issue number1-2
StatePublished - Jun 1 2006


  • COX-2
  • IBDV
  • NF-κB
  • Proinflammatory cytokines
  • p38MAPK

ASJC Scopus subject areas

  • Cancer Research
  • Virology
  • Infectious Diseases


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