Antagonism of eosinophil accumulation in asthma.
There is considerable evidence that implicates eosinophils as important effector cells and immunomodulators in the inflammation characteristic of asthma. Numerous in vitro and animal studies have demonstrated essential roles for cell adhesion molecules in eosinophil adhesion and transendothelial migration including the selectins, ICAM-1, VCAM-1 together with many of the 1 and β2 integrins. A large body of evidence has also implicated several cytokines and chemokines in the selective recruitment of eosinophils to sites of asthmatic inflammation. Biopharmaceutical approaches have been used to identify inhibitory molecules that target key elements in the processes controlling eosinophil accumulation in asthma. This review will summarise, the problems and successes regarding recent patents and developments in adhesion-based therapeutic strategies aimed at reducing eosinophil-mediated inflammation in the asthmatic lung.
Walsh
Garry M
GM
School of Medicine & Dentistry, Institute of Medical Sciences, University of Aberdeen, Scotland, UK. g.m.walsh@abdn.ac.uk
D018927:Anti-Asthmatic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors / Q000276:immunology*; D002465:Cell Movement / Q000187:drug effects; D055808:Drug Discovery; D004804:Eosinophils / Q000187:drug effects* / Q000276:immunology; D006801:Humans; D010330:Patents as Topic; D011014:Pneumonia
D018927:Anti-Asthmatic Agents; D015815:Cell Adhesion Molecules