权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Mechanism of immune regulation in the intestinal parasite infect models

肠道寄生虫感染模型的免疫调节机制

基本信息

批准号：
03454178
负责人：
TADA Isao
金额：
$ 3.39万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1992
项目状态：
已结题

项目摘要

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.

已知辅助性T细胞参与肠道寄生虫的免疫驱逐。在本研究中，我们研究了IL-5作为辅助性T细胞分泌的一种细胞因子在实验动物模型中的作用。v.），S. venezuelensis（S. v.）的和旋毛虫Trichinella spiralis（T.s.）。结果表明：1）IL-5是引起感染S.r.，S. v.和T.s.2）在小鼠S. v.感染中，如果在初次感染前3天接种抗IL-5单克隆抗体（NC 17），则与对照小鼠相比，虫负荷显著增加。然而，在这个过程中，嗜酸性粒细胞没有参与。在小鼠初次感染S.五，IL-5对小鼠的不应期和排异期均无影响。v.-感染的小鼠抵抗再感染，对移行幼虫的不应性是IL-5依赖性的，并且提供有IL-5受体的细胞在该机制中起作用。另一方面，在肠道阶段观察到的保护作用并不依赖于IL-5.4）在先前感染链球菌的小鼠中观察到针对SV幼虫攻击的交叉保护作用保护发生在小肠，但不是在迁移阶段。在该交叉保护实验中，施用NC 17显示部分阻断。感染小鼠，对新生幼虫的保护作用不形成重组IL-5。此外，给予小鼠NC 17对初次感染和再感染的保护作用均无影响。该研究揭示了IL-5的保护作用根据寄生虫的种类而存在差异。因此，这些证据将显示寄生的多样性进化方式逃避宿主的保护机制。