Persistent immune activation associated with a mouse model of Staphylococcus aureus-induced experimental brain abscess.
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-1 beta, 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.
Baldwin
Aaron C
AC
Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Slot 510 4301 W. Markham Street Little Rock, AR 72205, USA.
Kielian
Tammy
T
D000818:Animals; D001812:Blood-Brain Barrier / Q000473:pathology; D001922:Brain Abscess / Q000276:immunology* / Q000473:pathology / Q000821:virology; D054426:Chemokine CXCL2; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology*; D007375:Interleukin-1 / Q000096:biosynthesis; D051379:Mice; D015846:Monokines / Q000096:biosynthesis; D013203:Staphylococcal Infections / Q000276:immunology* / Q000473:pathology; D013211:Staphylococcus aureus / Q000276:immunology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D054426:Chemokine CXCL2; D007375:Interleukin-1; D015846:Monokines; D014409:Tumor Necrosis Factor-alpha