| Budget Amount *help |
¥5,300,000 (Direct Cost: ¥5,300,000)
Fiscal Year 1992: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1991: ¥3,800,000 (Direct Cost: ¥3,800,000)
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| Research Abstract |
It has been known that helper T cell is involved in the immunological expulsion of intestinal parasites. In the present study, we investigated the role of IL-5 as a cytokine secreted from helper T cells in the experimental animal models infected with Strongyloides ratti (S. v.), S. venezuelen-sis (S. v.) and Trichinella spiralis (T.s.). The following findings were obtained.
1) IL-5 is mainly responsible for the eosinophilia in the peripheral blood of the mice infected with each of S.r.,S.v. and T.s.
2) In the S.v. infection in mice, if anti-IL-5 monoclonal antibody (NC 17) was inoculated 3 days prior to the primary infection, the worm burden was markedly increased in comparison with the control mice. In this process, however, eosinophiles were not involved. In the primary infection of mice with S. v., IL-5 does not affect on the refractoriness nor expulsion.
3) In the protective mechanism of S. v.-infected mice against reinfection, the refractoriness against migrating larvae was IL-5 dependent and the cells provided with IL-5 receptors played a role in this mechanism. On the other hand, the protection seen in the intestinal phase did not depend on IL-5.
4) Cross protection against challenge with S.v. larvae was seen in mice which were previously infected with S.r. Protection occurred in the small intestine, but not in the migratory phase. In this cross protection experiment, the administration of NC 17 revealed partial blockade.
5) In the T.s. infected mice, protection against newborn larvae was not formed by recombinant IL-5. Further, administration of NC 17 to the mice did not affect on the protection against both the primary and reinfections.
The study revealed the diversity in the effect of IL-5 according to the species of parasites in term of protection. Thus, these evidences would show the diverse evolutionary way of parasitism by evading the host's protection mechanism.
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