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Retarded development of Schistosoma mansoni in immunosuppressed mice

Published online by Cambridge University Press:  06 April 2009

R. A. Harrison  and
M. J. Doenhoff
R. A. Harrison
Affiliation:
Department of Medical Helminthology, London School of Hygiene and Tropical Medicine, 395 Hatfield Road, St Albans, Herts AL4 0XQ
M. J. Doenhoff
Affiliation:
Department of Medical Helminthology, London School of Hygiene and Tropical Medicine, 395 Hatfield Road, St Albans, Herts AL4 0XQ
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Summary

Previous observations, which showed that treatment of mice with hydrocortisone acetate around the time of their infection with Schistosoma mansoni reduced the mature worm burden, have been confirmed. The number of eggs produced by the surviving worms during early patency was also significantly reduced. Cyclophosphamide and another steroid immunosuppressant, betamethasone, also caused a reduction in fecundity of S. mansoni when given at the time of infection, as did T-cell deprivation of the mice by adult thymectomy and injection of anti-thymocyte serum 1 month before infection. There was no effect of these three treatments on worm numbers. In contrast, injection of mice with anti-thymocyte serum at the time of infection marginally increased the size of the mature worm burden. The deleterious effects of hydrocortisone acetate on S. mansoni worm numbers and fecundity were only apparent if the steroid was given within 1 week of infection. Indomethacin, a compound which inhibits tissue inflammatory reactions by inhibiting prostaglandin synthesis, and which therefore mimics one of the actions of corticosteroids, had no effect on S. mansoni worm maturation and fecundity.

Type
Research Article
Information
Parasitology , Volume 86 , Issue 3 , June 1983 , pp. 429 - 438
Copyright
Copyright © Cambridge University Press 1983

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