Deficiency of CD18 gene reduces brain edema in experimental intracerebral hemorrhage in mice.

Experimental studies of intracerebral hemorrhage (ICH) point toward leukocytes as a major contributor to ICH-induced brain injury. Leukocyte and endothelial cell adhesion molecules are responsible for injurious neutrophil-endothelial cell interactions in vasculature. Since deficiency of leukocyte-expressed CD18 protects against ischemia-reperfusion injury, we hypothesized that such deficiency may have similar effect in ICH-induced injury. Our aim was to investigate whether CD18 deficiency affords neuroprotection by decreasing ICH-induced brain injury, thereby improving neurological function and reducing mortality. A total of 20 males wild-type CDI8+/+ mice and 12 CD18-/- knockout mice were used in our study. ICH was induced by collagenase injection. Mortality, neurological function, and brain edema were measured at 24h after ICH. Data were analyzed by ANOVA, Chi-square, and Student t-test. Differences of p < 0.05 were considered statistically significant. Our study showed that the increase in brain water content caused by ICH was significantly smaller in CD18 knockout mice compared with wild-type mice (p < 0.05, Student t-test). This result correlated with a tendency toward improvement of neurological function and a decrease in mortality. We conclude that CD18 deficiency significantly reduces brain edema after ICH, which corresponds with a trend toward reduction in neurological deficit and mortality.