Neutrophil adhesion and the therapy of inflammation.
Cell adhesion has an essential role in neutrophil recognition of sites of inflammation, migration through endothelium and extracellular matrix, and activation to full effector function at these sites. Adhesion molecules on the neutrophil involved in these events include members of the selectin, integrin, and immunoglobulin superfamilies. Inhibition of neutrophil adhesion holds the promise of interrupting idiopathic inflammation in a variety of diseases, but also can increase susceptibility to infection. The therapeutic challenge is to design agents of sufficient specificity to block the deleterious effects of neutrophil influx and activation without interference with host defense. This will require improved understanding of the molecular events regulating, and regulated by, neutrophil adhesion.
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Division of Infectious Diseases, Washington University School of Medicine, St Louis, MO 63110, USA.
D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology*; D002465:Cell Movement; D005109:Extracellular Matrix; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000473:pathology; D016023:Integrins / Q000502:physiology; D009504:Neutrophils / Q000473:pathology / Q000502:physiology*; D019087:Selectins / Q000502:physiology
D016023:Integrins; D019087:Selectins