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Eosinophilia, parasite burden and lung damage in Toxocara canis infection in C57Bl/6 mice genetically deficient in IL‐5
Author(s) -
TAKAMOTO M.,
OVINGTON K. S.,
BEHM C. A.,
SUGANE K.,
YOUNG I. G.,
MATTHAEI K. I.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00208.x
Subject(s) - eosinophilia , toxocara canis , biology , embryonated , canis , immunology , toxocariasis , pulmonary eosinophilia , interleukin 5 , bone marrow , interleukin , eosinophil , cytokine , helminths , inoculation , paleontology , asthma
C57Bl/6 mice genetically deficient in interleukin (IL)‐5 (IL‐5 −/− ) and mice with the normal IL‐5 gene (IL‐5 +/+ ) were infected with embryonated eggs of Toxocara canis. IL‐5 +/+ mice developed a marked eosinophilia in their peripheral bloods and bone marrows after infection. In contrast, the number of eosinophils at these sites actually decreased during the acute phase of infection in IL‐5 −/− mice. A smaller number of eosinophils infiltrated the lung, liver, heart and skeletal muscle of infected IL‐5 −/− mice than those of infected IL‐5 +/+ mice. Eosinophils were not produced incultures of bone marrow cells from either IL‐5 +/+ or IL‐5 −/− mice which were stimulated with excretory–secretory antigen of T. canis larvae. The capacity of cells from the bone 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 an IL‐5‐like molecule is not produced by the T. canis larvae and that IL‐5 produced by host cells is solely responsible for the eosinophilia in mice infected with this nematode. The number and location of T. canis larvae were not altered in the absence of IL‐5. In contrast, lung damage in infected IL‐5 −/− mice was less extensive than that in infected IL‐ 5 +/+ mice, although structures resembling Charcot–Leyden crystals were seen in the lungs of both IL‐5 +/+ and IL‐5 −/− mice. These results suggest that eosinophils play a role in the pathology in mice infected with T. canis .