To examine the significance of chemokine activation of CXCR2 in wound healing 
after chemical burn, cutaneous injury was created by topical application of 
nitrogen mustard on CXCR2 wild type (+/+), heterozygous (+/-), and knockout 
(-/-) mice. Wounds were analyzed histologically for neutrophil and monocyte 
infiltration and for reepithelialization at postwound days 4, 7, and 10. 
Neutrophil recruitment to the wound site was reduced through postwound day 7 in 
CXCR2 -/- mice as indicated by myeloperoxidase assay and by visual quantitation. 
Because there is always concern that mice with targeted deletion of a specific 
receptor may undergo developmental adaptations to offset the loss of the 
receptor, we also accessed chemical wound repair in the presence of a small 
molecule antagonist of CXCR2. Dietary supplementation with a CXCR2 antagonist 
(SB-265610) during the wound repair process also markedly delayed healing 
parameters in CXCR2 +/+ mice, even greater than treatment with glucocorticoids. 
These parallel studies further establish that mice deficient in CXCR2 function 
exhibit delayed cutaneous wound healing that may be primarily linked to impaired 
neutrophil recruitment after chemical burn with nitrogen mustard. Thus, there 
may be a potential therapeutic benefit of treating nitrogen mustard-induced skin 
lesions with agonists of CXCR2 to facilitate the wound repair process.