# Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke

## TL;DR

This study finds that neutrophils are not a major source of gelatinase activity or brain damage after a stroke.

## Contribution

The study demonstrates that neutrophils are not a significant contributor to gelatinase activity or acute brain damage after stroke.

## Key findings

- Neutrophil depletion did not reduce gelatinase (MMP-2 and MMP-9) expression or activity after stroke.
- Neutrophil depletion had no effect on edema, hemorrhage, or infarct size.
- Gelatinase activity increases after stroke even without circulating neutrophils.

## Abstract

While gelatinase (MMP-2 and -9) activity is increased after focal ischemia/reperfusion injury in the brain, the relative contribution of neutrophils to the MMP activity and to the development of hemorrhagic transformation remains unknown.

Anti-PMN treatment caused successful depletion of neutrophils in treated animals. There was no difference in either infarct volume or hemorrhage between control and PMN depleted animals. While there were significant increases in gelatinase (MMP-2 and MMP-9) expression and activity and edema formation associated with ischemia, neutrophil depletion failed to cause any change.

The main finding of this study is that, in the absence of circulating neutrophils, MMP-2 and MMP-9 expression and activity are still up-regulated following focal cerebral ischemia. Additionally, neutrophil depletion had no influence on indicators of ischemic brain damage including edema, hemorrhage, and infarct size. These findings indicate that, at least acutely, neutrophils are not a significant contributor of gelatinase activity associated with acute neurovascular damage after stroke.