The expression of the chemokines macrophage inflammatory protein (MIP)-2 an
d MIP-1 alpha and of their receptors CXCR2 and CCR5 was assessed in wild ty
pe (WT) and TNF/lymphotoxin-alpha knockout (TNF/LT-alpha-/-) mice subjected
to closed head injury (CHI). At 4 h after trauma intracerebral MIP-2 and M
IP-1 alpha levels were increased in both groups with MIP-2 concentrations b
eing significantly higher in WT than in TNF/LT-alpha-/- animals (p<0.05). T
hereafter, MIP-2 production declined rapidly, whereas MIP-1<alpha> remained
elevated for 7 days. Expression of CXCR2 was confined to astrocytes and in
creased dramatically within 24 h in both mouse types. Contrarily, CCR5 expr
ession remained constitutively low and was mainly localized to microglia. T
hese results show that after CHI, chemokines and their receptors are regula
ted differentially and with independent kinetics. NeuroReport 12:2059-2064
(C) 2001 Lippincott Williams & Wilkins.