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Immune response impairment, genotoxicity and morphological transformation induced by Taenia solium metacestode
L A Herrera1, P Santiago, G Rojas
1Instituto de Investigaciones Biomédicas, UNAM, Ciudad Universitaria, México, D.F., Mexico.
Abstract:
In chronic helminthic infections such as cysticercosis, where the parasites live for years, profound modulation of the host immune response has been reported. To evaluate the genotoxicity of a drug used to treat cysticercosis, we observed the occurrence of genetic damage in cultured lymphocytes from cysticercotic swine and patients who had not been exposed to the drug. The human lymphocytes also showed a slower proliferation. These data suggested that the disease itself was promoting genetic damage in host lymphocytes which, in part, could explain the retardation of the lymphocyte proliferation observed in cysticercotic patients. Pigs infected with Taenia solium cysticerci showed an increased lymphocyte proliferation for 6-8 weeks post infection, followed by an impaired proliferation after this period. Significant induction of sister-chromatid exchanges was also observed in lymphocytes from infected pigs after the 6th week post infection. Additionally, it was found that a factor secreted by the cysticerci morphologically transformed primary fibroblasts in culture. The results strongly suggest that the parasite produces genetic instability in the host cells, which could result in immunosuppression and malignant transformation of target cells.
Insights
The parasite causing cysticercosis induces genetic damage and instability in host immune cells, potentially leading to immunosuppression and cancer. This occurs independently of any drug treatment.
Area of Science:
- Immunology
- Genetics
- Parasitology
Background:
- Chronic helminthic infections like cysticercosis involve significant host immune modulation.
- The long-term presence of parasites can alter host cell behavior and genetic stability.
- Previous studies indicated profound immune response changes in helminthic infections.
Purpose of the Study:
- To investigate the genotoxicity of a cysticercosis treatment drug.
- To evaluate genetic damage in lymphocytes from infected swine and patients.
- To understand the disease's impact on host cell proliferation and genetic integrity.
Main Methods:
- Cultured lymphocytes from cysticercotic swine and patients were analyzed for genetic damage.
- Lymphocyte proliferation rates were measured in infected and control subjects.
- Sister-chromatid exchanges were assessed in lymphocytes from infected pigs.
- Fibroblast cultures were exposed to factors secreted by cysticerci.
Main Results:
- The disease itself, not the drug, induced genetic damage in host lymphocytes.
- Human lymphocytes from patients showed slower proliferation.
- Pigs exhibited impaired lymphocyte proliferation and increased sister-chromatid exchanges post-infection.
- Parasite-secreted factors transformed primary fibroblasts in culture.
Conclusions:
- Cysticercosis infection promotes genetic instability in host cells.
- This genetic instability may contribute to immunosuppression.
- The findings suggest a link between parasitic infection, genetic damage, and potential malignant transformation.