Chemokines and the inflammatory response following cardiopulmonary bypass--a new target for therapeutic intervention?--A review

Abstract

This 10-year Medline search of English-language articles describing experimental and clinical studies on chemokines, cardiopulmonary bypass (CPB) and systemic or multiorgan failure revealed that chemokines are significantly involved in the pathogenesis of post-CPB syndrome. The post-CPB inflammatory response depends upon recruitment and activation of inflammatory cells. Leucocyte recruitment is a well-orchestrated process that involves several protein families, including pro-inflammatory cytokines, adhesion molecules and chemokines. Current anti-inflammatory therapies mostly act on the cells that have already been recruited. A more efficient therapy might be the prevention of excessive recruitment of particular leucocyte populations by antagonizing chemokine receptors which might act upstream of the current anti-inflammatory agents. The chemokines, which are a cytokine subfamily of chemotactic cytokines, participate in recognizing, recruiting, removing and repairing inflammation. As chemokines target specific leucocyte subsets, antagonism of a single chemokine ligand or receptor would be expected to have a circumscribed effect, thereby endowing the antagonist with a limited side-effect profile. Chemokines should be considered as possible targets for therapeutic intervention.