A rapid and transient peripheral inflammatory response precedes brain inflammation after experimental stroke.
Increasing evidence suggests that peripheral inflammatory responses to stroke and other brain injuries have an important role in determining neurological outcome. The mediators of this response and the temporal relationships between peripheral and central inflammatory alterations are poorly understood. In this study, we show that experimental stroke in mice induces a peripheral inflammatory response that peaks 4 h after stroke, and precedes the peak in brain inflammation 24 h after stroke. This peripheral response is dominated by the induction of the chemokine CXCL-1 and the proinflammatory cytokine interleukin-6 and could serve as an accessible target for therapy and as a source of biomarkers predictive of prognosis.
Chapman
Katie Z
KZ
Faculty of Life Sciences, University of Manchester, Manchester, UK.
Dale
Verity Q
VQ
Dénes
Adám
A
Bennett
Gavin
G
Rothwell
Nancy J
NJ
Allan
Stuart M
SM
McColl
Barry W
BW
D000818:Animals; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology / Q000276:immunology* / Q000378:metabolism; D015850:Interleukin-6 / Q000096:biosynthesis* / Q000097:blood; D016209:Interleukin-8 / Q000096:biosynthesis* / Q000097:blood; D051379:Mice; D008810:Mice, Inbred C57BL; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020521:Stroke / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D013997:Time Factors; D015854:Up-Regulation
D015850:Interleukin-6; D016209:Interleukin-8