Human cellular inflammation in the pathology of acute cerebral ischaemia
- 1Department of Medicine, Addenbrooke’s Hospital, Cambridge, UK
- 2Division of Stroke Medicine, Addenbrooke’s Hospital
- 3Anaesthesia, University of Cambridge
- Correspondence to: Dr Christopher J S Price, Box 83 (R3 Neuroscience), Addenbrooke’s Hospital, Cambridge CB22QQ, UK; cp252medschl.cam.ac.uk
- Received 19 December 2002
- Accepted 9 June 2003
- Revised 23 May 2003
Abstract
Leucocytes form important effector pathways for inflammation. This article reviews the clinical evidence for the presence of a cellular inflammatory response in cerebral ischaemia, and attempts to define its temporal profile and spatial distribution. The processes involved in recruitment and activation of leucocytes in this context are addressed, and the successes and failures of interventions aimed at these processes discussed.
- CINC, cytokine induced neutrophil chemoattractant
- ELISA, enzyme linked immunosorbent assay
- HMPAO, hexamethylpropylene amine oxime
- ICAM, intercellular adhesion molecule
- IL, interleukin
- MCP, monocyte chemoattractant protein
- MIP, macrophage inflammatory protein
- MMP, matrix metalloproteinase
- NAP, neutrophil activating protein
- PBBS, peripheral-type benzodiazepine binding site
- PET, positron emission tomography
- PSGL, P-selectin glycoproteins ligand
- RANTES, regulated on activation normal T cell expressed and secreted
- RNA, ribonucleic acid
- SDF, stromal cell derived factor
- SLC, secondary lymphoid tissue chemokine
- SPECT, single photon emission tomography
- TIA, transient ischaemic attack
- TNF, tumour necrosis factor
- VCAM, vascular cell adhesion molecule
Footnotes
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Competing interests: none declared
