Retarded development of Schistosoma mansoni in immunosuppressed mice

Abstract

SUMMARYPrevious 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.