Summary
Chemokine signaling plays an important role in the postischemic inflammatory response.
Overlapping pathways involving reactive oxygen intermediates,Toll-like receptor (TLR)
activation, the complement cascade and the nuclear factor (NF)- κ B system induce
both CXC and CC chemokines in ischemic tissues. Reperfusion accentuates chemokine
expression promoting an intense inflammatory reaction. ELR-containing CXC chemokines
regulate neutrophil infiltration in the ischemic area, whereas CXCR3 ligands may mediate
recruitment of Th1 cells. CC chemokines, on the other hand, induce mononuclear cell
infiltration and macrophage activation.Evidence suggests that chemokine signaling
mediates actions beyond leukocyte chemotaxis and activation, regulating angiogenesis
and fibrous tissue deposition. Effective repair of ischemic tissue is dependent on
a wellorchestrated cellular response and on timely induction and suppression of chemokines
in a locally restricted manner. This manuscript reviews the evidence suggesting a
role for chemokine- mediated effects in ischemia/reperfusion and discusses the potential
significance of these interactions in injury and repair of ischemic tissues.
Keywords
Chemokine - ischemia - reperfusion - leukocyte - inflammation