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- W1577894157 abstract "Leukocytes are an integral component of the host defense system. However, in some disease states their action may instead be deleterious to the host and they may cause a significant amount of tissue damage. For example, in ischemia-reperfusion (I-R) injury an ischemic insult may trigger an inflammatory response during reperfusion that causes more injury than the initial ischemic insult. In other diseases, such as rheumatoid arthritis, leukocytes cause tissue damage without an apparent initial insult. In still other instances, leukocytes may function normally, but it is advantageous to manipulate their function. In order for leukocytes to cause vascular or tissue damage, they must first adhere to the endothelium and then exit the bloodstream to gain access to extravascular tissue. Leukocyte emigration involves adhesion molecules both on the leukocyte and on the endothelial cell surface. These adhesion molecules are vital not only for adherence but participate in several other leukocyte functions such as signal transduction. Therefore, adherence molecules have emerged as important targets for therapy in a broad spectrum of inflammatory and immune disorders. This chapter reviews the current status of “anti-adhesion’’ therapy in a number of in vivo models of disease states and considers some of the safety concerns associated with anti- adhesion therapy. The chapter discusses the relation between leukocyte and endothelial adhesion molecules—selectins, integrins and immunoglobulin superfamily—adhesion cascade and inflammation, strategies to inhibit adhesion, ischemia- reperfusion injury of the various selectins, oligosaccharides and the various integrins. There are details on atherosclerosis—adhesion molecule expression, anti-adhesion therapy—thermal injury, arthritis, asthma, organ transplantation, acute lung injury, multiple sclerosis and other miscellaneous diseases. Blocking either the initial rolling of leukocytes along the endothelium or the firm adherence of leukocytes to the endothelium has been found to be effective in reducing leukocyte-mediated injury and leukocyte accumulation." @default.
- W1577894157 created "2016-06-24" @default.
- W1577894157 creator A5075290824 @default.
- W1577894157 creator A5082034991 @default.
- W1577894157 creator A5082745011 @default.
- W1577894157 date "1997-01-01" @default.
- W1577894157 modified "2023-10-16" @default.
- W1577894157 title "Anti-adhesion Therapy" @default.
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