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Introduction: The Role of Inflammation in Mediating Damage Following Stroke and Neurotrauma

Till recently little consideration was given to inflammation as playing a role in contributing to damage following stroke and neurotrauma. But this has changed. A search of Pub Med revealed that 909 articles are brought up with the key words stroke and inflammation; 383 with the key words brain trauma and inflammation; and 297 with the key words spinal cord trauma and inflammation. The 5 Altschul Symposium (The Role of Inflammation in Mediating Damage Following Stroke and Neurotrauma), held August 19-21, 1999, at the University of Saskatchewan, Saskatoon, Saskatchewan, Canada addressed the topic of inflammation in stroke and neurotrauma in some depth. The first paper by del Zoppo and colleagues gives a comprehensive overview of inflammation in stroke, discussing pro-inflammatory cytokines, chemokines, enzymes and cell adhesion molecules. This paper starts off with the important focus of the dynamic microvascular changes during ischemia and reperfusion. Since the endothelium regulates what enters the CNS parenchyma, it becomes an obvious target for therapeutic intervention. Experimental therapies directed towards interfering with leukocyte entry are discussed as well as therapies directed towards inhibition of expression of pro-inflammatory genes. Stanimirovic and Satoh focus on what is known about the mediators of inflammatory gene expression in the cerebral microvascular endothelium. Discussed are the role of the autocoids, prostaglandins, leukotrienes, platelet-activating factor; cytokines/chemokines; and the modulation of pro-inflammatory gene expression. Kubes and Ward discuss the role of cell adhesion molecules in leukocyte recruitment and how this may vary from the microvascular bed of one tissue to another. Katoh and Walz examine the rapid morphological and electrophysiological responses of microglia to ischemic insults. Brain temperature affects the outcome of stroke. Hypothermia as a protective mechanism and the consequence of infection-related hyperthermia is dealt with by Corbett and Thornhill. The final paper by Christman and colleagues examines the role of the transcription factor complex, NF B in promoting pro-inflammatory gene expression. Discussed is the evidence for reactive oxygen species playing a role in the signal transduction cascade that activates NF B. Also discussed is the potential of phase II enzyme inducers to minimize oxidative stress. Minimizing oxidative stress should decrease the chances of activating NF B and, hence, ameliorating the inflammatory response. Although there was a brief discussion on some of the possible downstream neuroprotective consequences of the pro-inflammatory cytokine TNF , the emphasis of this Symposium has been the deleterious effect of inflammation, in particular the neutrophil-mediated inflammatory responses. There is evidence accumulating that components, particularly the delayed components, of the inflammatory response may be beneficial for repair processes and the reader is directed to a recent review by Schwartz and colleagues (1).