Mice lacking the chemokine receptor CCR1 show increased susceptibility to Toxoplasma gondii infection

Chemokines are critical for the recruitment of effector immune cells to sit es of infection. Mice lacking the chemokine receptor CCR1 have defects in n eutrophil trafficking and proliferation. In the present study, we tested th e susceptibility of CCR1 knockout mice to infection with the obligate intra cellular protozoan parasite Toxoplasma gondii. In comparison with parental wild-type mice, CCR1(-/-) mice exhibited dramatically increased mortality t o T. gondii in association with an increased tissue parasite load. No diffe rences were observed in Ag-specific T cell proliferation or in cytokine res ponses between mutant and wild-type mice. However, the influx of PMNs to th e peripheral blood and to the liver were reduced in CCR1(-/-) mice during e arly infection. Our results suggest that CCR1-dependent migration of neutro phils to the blood and tissues may have a significant impact in controlling parasite replication.