Modulation of immunity in mice with latent toxoplasmosis--the experimental support for the immunosuppression hypothesis of Toxoplasma-induced changes in reproduction of mice and humans
Language English Country Germany Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Asymptomatic Infections * MeSH
- Immune Tolerance * MeSH
- Interleukin-10 metabolism MeSH
- Interleukin-12 metabolism MeSH
- Humans MeSH
- Lymphocytes immunology MeSH
- Disease Models, Animal MeSH
- Mice MeSH
- Nitric Oxide metabolism MeSH
- Cell Proliferation MeSH
- Reproduction physiology MeSH
- Toxoplasma immunology MeSH
- Toxoplasmosis complications immunology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Interleukin-10 MeSH
- Interleukin-12 MeSH
- Nitric Oxide MeSH
The immunosuppression hypothesis suggests that the increased sex ratio in mice and women with latent toxoplasmosis, retarded embryonic growth in the early phases of pregnancy, prolonged pregnancy of Toxoplasma-infected women, and increased prevalence of toxoplasmosis in mothers of children with Down syndrome can be explained by the presumed immunosuppressive effects of latent toxoplasmosis. Here, we searched for indices of immunosuppression in mice experimentally infected with Toxoplasma gondii. Our results showed that mice in the early phase of latent infection exhibited temporarily increased production of interleukin (IL)-12 and decreased production of IL-10. In accordance with the immunosuppression hypothesis, the mice showed decreased production of IL-2 and nitric oxide and decreased proliferation reaction (synthesis of DNA) in the mixed lymphocyte culture in the early and also in the late phases of latent toxoplasmosis. Since about 30% of the world population are latently infected by T. gondii, the toxoplasmosis-associated immunosuppression might have serious public health consequences.
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