EOSINOPHILIA, PARASITE BURDEN AND LUNG DAMAGE IN TOXOCARA-CANIS INFECTION IN C57BL 6 MICE GENETICALLY DEFICIENT IN IL-5/

C57B1/6 mice genetically deficient in interleukin (IL)-5 (IL-5(-/-)) a nd mice with the normal IL-5 gene (IL-5(+/+)) were infected with embry onated eggs of Toxocara canis. IL-5(+/+) mice developed a marked eosin ophilia in their peripheral bloods and bone marrows after infection. I n contrast, the number of eosinophils at these sites actually decrease d during the acute phase of infection in IL-5(-/-) mice. A smaller num ber of eosinophils infiltrated the lung, liver, heart and skeletal mus cle of infected IL-5(-/-) mice than those of infected IL-5(+/+) mice. Eosinophils were not produced in cultures of bone marrow cells from ei ther IL-5(+/+) or IL-5(-/-) mice which were stimulated with excretory- secretory antigen of T. canis larvae. The capacity of cells from the b one marrow to differentiate into eosinophils when stimulated in vitro with recombinant murine IL-5 was the same whether the cells were from IL-5(+/+) or IL-5(-/-) mice. Taken together, these results show that a n IL-5-like molecule is not produced by the T. canis larvae and that I L-5 produced by host cells is solely responsible for the eosinophilia in mice infected with this nematode. The number and location of T. can is larvae were not altered in the absence of IL-5. In contrast, lung d amage in infected IL-5(-/-) mice was less extensive than that in infec ted IL-5(+/+) mice, although structures resembling Charcot-Leyden crys tals were seen in the lungs of both IL-5(+/+) and IL-5(-/-). mice. The se results suggest that eosinophils play a role in the pathology in mi ce infected with T. canis.