This study was undertaken to evaluate the role of
IL-5 in eosinophil migration and in the maintenance of
eosinophilia in a guinea-pig model of
visceral larva migrans syndrome. The results show that the
infection of animals with Toxocara canis induced an early increase in serum
IL-5 levels that might be essential for eosinophil differentiation and proliferation and for the development of
eosinophilia. When infected guinea-pigs were treated with mAb anti-IL-5 (TRFK-5) given at the same time or 1 or 3 days after
infection, there was a high percentage of reduction of eosinophil counts 18 days after
infection. However, when the mAb was administered during the peak of
eosinophilia, there was high inhibition in blood, no inhibition in bronchoalveolar lavage fluid (BALF) or peritoneum and an increase in eosinophil numbers in bone marrow. Thus, a basic level of
IL-5 may be essential to drive eosinophils from bone marrow to blood and tissues, and for the maintenance of
eosinophilia in infected animals. We may also conclude that when eosinophils have already migrated to the lungs, TRFK-5 has no power to inhibit
eosinophilia, which is also under control of local lung cells producing
IL-5. In this way, only one later TRFK-5 treatment may not be sufficient to modify the lung parenchyma microenvironment, since T. canis
antigens had already stimulated some cell populations to produce
IL-5.