Accumulation of microglial cells expressing ELR motif-positive CXC chemokines and their receptor CXCR2 in monkey hippocampus after ischemia-reperfusion.

ELR(+) CXC chemokines including IL-8 are known to be involved in the ischemia-reperfusion injuries in various organs including rodent brain. However, the roles of these chemokines during the ischemia-reperfusion injuries of the primate brain still remain unknown. Here, we studied expressions of CXC chemokines and their receptor CXCR2 in monkey hippocampus known to develop total CA1 neuronal loss on day 5 after 20-min ischemia and reperfusion. ELR(+) chemokines and their receptor CXCR2 were not detected in the hippocampus of non-ischemic monkeys. On the contrary, at 30-60 min after the start of reperfusion, CD68-positive microglial cells increased significantly in the hippocampal CA1 sector, but there was negligible infiltration of neutrophils. These microglial cells expressed simultaneously growth regulated oncogene (Gro)-alpha and other ELR(+) CXC chemokines. Moreover, CD68-positive microglial cells also expressed the receptor for ELR(+) CXC chemokines. On day 4, capillary endothelial cells were significantly increased in the CA1 sector. Considering that ELR(+) CXC chemokines have potent angiogenic activities, the coordinate expression of ELR(+) CXC chemokines and their receptor CXCR2 in microglial cells may be related not only to the ischemic brain injuries but also to the microglial and capillary proliferation in the monkey hippocampus.