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*
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and
Departamento de Patologia Animal (Microbiologia e Immunologia), Facultad de Veterinaria, Universidad de Murcia, Murcia, Spain
Neutrophil migration to the site of infection is a critical early
step in host immunity to microbial pathogens, in which chemokines and
their receptors play an important role. In this work, mice deficient in
expression of the chemokine receptor CXCR2 were infected with
Toxoplasma gondii and the outcome was monitored.
Gene-deleted animals displayed completely defective neutrophil
recruitment, which was apparent at 4 h and sustained for at least
36 h.
KitW/KitW-v
animals also displayed defective polymorphonuclear leukocyte
migration, suggesting mast cells as one source of chemokines driving
the response. Tachyzoite infection and replication were accelerated in
CXCR2-/- animals, resulting in establishment of higher
cyst numbers in the brain relative to wild-type controls. Furthermore,
serum and spleen cell IFN-
levels in infected, gene-deleted mice
were reduced 60–75% relative to infected normal animals, and spleen
cell TNF-
was likewise reduced by 
50%. These results highlight
an important role for CXCR2 in neutrophil migration, which may be
important for early control of infection and induction of immunity
during Toxoplasma infection.
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