Inflammation in stroke: the good, the bad, and the unknown.

Abstract

It has been known for a very long time (Spielmeyer 1922) that in ‘apoplectic’ brains the hallmarks of inflammation may be found, including pus-filled cavities. Until very recently it was generally believed that brain inflammation following stroke is a secondary reaction to the destruction of brain tissue, which is cleared by invading leukocytes, in particular macrophages (Manoonkitiwongsa et al. 2001). Accordingly, inflammation is supposed to free the brain from the debris of dead cells, but in itself does not participate in ischemic cell damage. Quite clearly, this concept must be modified in view of recent research. Numerous experimental as well as clinical studies have linked stroke-induced brain inflammation to the acute and delayed evolution of brain infarction, as well as to scattered selective neuronal injury in the infarct perimeter. These studies have been reviewed (e.g., Barone and Feuerstein 1999; del Zoppo et al. 2000, 2001; Kumar 2001; Iadecola and Alexander 2001; Emsley and Tyrrell 2002; Frijns and Kappelle 2002; Danton and Dietrich 2003) and we wrote an overview entitled ‘Inflammation in Stroke — A Potential Target for Neuroprotection’ (Priller and Dirnagl 2002) for the 2001 Ernst Schering Foundation Workshop ‘Neuroinflammation — From Bench to Bedside.’