Persistent immune activation associated with a mouse model of Staphylococcus aureus-induced experimental brain abscess

Aaron C. Baldwin, Tammy Kielian

Research output: Contribution to journalArticle

57 Scopus citations


We have established a mouse experimental brain abscess model using Staphylococcus aureus where lesion sites are greatly exaggerated compared to the localized area of initial infection, reminiscent of an overactive immune response. Here we demonstrate the prolonged expression of IL-1β, TNF-α, and macrophage inflammatory protein-2 (MIP-2/CXCL2), concomitant with a chronic disruption of the blood-brain barrier (BBB) in mice with S. aureus-induced brain abscess. These changes correlated with the continued presence of infiltrating neutrophils and macrophages/microglia. Collectively these findings suggest that the excessive tissue damage that often results from brain abscess may be mediated, in part, by the perpetuation of antibacterial immune responses that are not downregulated in a timely manner.

Original languageEnglish (US)
Pages (from-to)24-32
Number of pages9
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - Jun 1 2004



  • Brain abscess
  • Chemokines
  • Cytokines
  • Glia
  • Neuroimmunology
  • Staphylococcus aureus

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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