Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 151, Issue 1-2, Pages 24-32Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2004.02.002
Keywords
brain abscess; Staphylococcus aureus; chemokines; cytokines; glia; neuroimmunology
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Funding
- NIMH NIH HHS [MH65297] Funding Source: Medline
- NINDS NIH HHS [R01 NS40730] Funding Source: Medline
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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-1beta, TNF-alpha, 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. (C) 2004 Elsevier B.V. All rights reserved.
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