Premium
Neutrophil activation during reperfusion after ischemic stroke in mice
Author(s) -
Morrison Helena Willington,
DavisGorman Grace,
Frye Jennifer,
McDonagh Paul,
Funk Janet,
Ritter Leslie
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.615.1
Subject(s) - medicine , reperfusion injury , stroke (engine) , ischemia , anesthesia , microcirculation , cerebral blood flow , integrin alpha m , flow cytometry , blood flow , middle cerebral artery , pharmacology , immunology , mechanical engineering , engineering
Experimental evidence in non‐murine models suggests that activated neutrophils play a pivotal role in cerebral reperfusion injury. Neutrophils release toxic mediators as they initially adhere to the microcirculation and migrate out of the circulation into to brain tissue. In this study we investigated whether systemic neutrophils are activated in mice during the first minutes and 24 hours after reperfusion following ischemic stroke. The filament method of middle cerebral artery occlusion (60 min) and reperfusion (MCAOR) was performed in male C57Bl/6J mice (22‐25g). Blood was drawn from the aorta after 15 minutes (MCAOR 15min, n=6) or 24 hours of reperfusion (MCAOR 24hr, n=2) and compared to blood obtained from a sham surgery (Sham, n=4). Neutrophil CD11b expression was measured in whole blood using flow cytometry methods. Compared to the shams, there was a 70% increase in neutrophil CD11b expression following MCAOR at 15 min ( p = 0.06) and a 108% increase following MCAOR at 24 hours ( p = 0.03). There was also an 83% and 94% increase of LPS‐stimulated neutrophil CD11b expression at 15 min ( p = 0.08) and 24 hours ( p = 0.13) of reperfusion. These results indicate that in a mouse model of MCAOR, systemic neutrophils 1) are activated and primed during the first minutes and after 24 hours of reperfusion, and 2) can be easily monitored to assess the effects of new treatments for reperfusion injury after stroke. Supported by NIH NRSA 1 F31 NR010658 ‐01 (Morrison) NIH HL 58859 (McDonagh) University of Arizona Emmons (Ritter)