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*
Department of Microbiology and Immunology, University of Adelaide, Adelaide, Australia; and
Biomedical Research Center, University of British Columbia, Vancouver, British Columbia, Canada
In this study, we have examined the ability of chemokine receptor
antagonists to prevent neutrophil extravasation in the mouse. Two
murine CXC chemokines, macrophage-inflammatory protein (MIP)-2 and KC,
stimulated the accumulation of leukocytes into s.c. air pouches,
although MIP-2 was considerably more potent. The leukocyte infiltrate
was almost exclusively neutrophilic in nature. A human CXC chemokine
antagonist, growth-related oncogene (GRO)-
(8–73), inhibited calcium
mobilization induced by MIP-2, but not by platelet-activating factor in
leukocytes isolated from the bone marrow, indicating that this
antagonist inhibits MIP-2 activity toward murine leukocytes.
Pretreatment of mice with GRO(8–73) inhibited, in a dose-dependent
manner, the MIP-2-induced influx of neutrophils to levels that were not
significantly different from control values. Moreover, this antagonist
was also effective in inhibiting the leukocyte recruitment induced by
TNF-, LPS, and IL-1ß. Leukocyte infiltration into the peritoneal
cavity in response to MIP-2 was also inhibited by prior treatment of
mice with GRO(8–73) or the analogue of platelet factor 4,
PF4(9–70). The results of this study indicate 1) that the murine
receptor for MIP-2 and KC, muCXCR2, plays a major role in neutrophil
recruitment to s.c. tissue and the peritoneal cavity in response to
proinflammatory agents and 2) that CXCR2 receptor antagonists prevent
acute inflammation in vivo.
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