Schistosoma Mansoni Infections in T-cell Deprived Mice, and the Ameliorating Effect of administering Homologous Chronic Infection Serum

I. Pathogenesis

M. DoenhoffDepartment of Medical Helminthology, London School of Hygiene and Tropical Medicine, Winches Farm Field Station, 395 Hatfield Road, St. Albans AL4 0XQ, England

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R. MusallamDepartment of Medical Helminthology, London School of Hygiene and Tropical Medicine, Winches Farm Field Station, 395 Hatfield Road, St. Albans AL4 0XQ, England

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J. BainDepartment of Medical Helminthology, London School of Hygiene and Tropical Medicine, Winches Farm Field Station, 395 Hatfield Road, St. Albans AL4 0XQ, England

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A. McGregorDepartment of Medical Helminthology, London School of Hygiene and Tropical Medicine, Winches Farm Field Station, 395 Hatfield Road, St. Albans AL4 0XQ, England

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Schistosoma mansoni-infected mice which were deprived of their T-cells by means of thymectomy and administration of antithymocyte serum have been shown to survive for a shorter time than similarly-infected, immunologically-intact controls. A marked blood polymorphonuclearcytosis was induced by the infection in deprived mice, with no concomitant eosinophilia. Intact mice responded to the infection with a moderate eosinophilia. In intact mice there was a substantial increase in spleen and mesenteric lymph node weights between 40 and 50 days after infection, whereas the lymphoid organ weights of infected deprived mice remained relatively constant from 30–50 days. Serum transaminase concentrations (SGOT and SGPT) increased from day 40 after infection of immunologically intact mice, but had returned to more normal levels by day 70. In infected, T-cell deprived mice SGOT and SGPT concentrations were markedly elevated between 40 and 60 days after infection when compared with infected, immunologically intact controls, this phenomenon being a probable correlate of S. mansoni-induced damage to liver parenchymal tissue in the former animals. Although there were no consistent differences between normal and deprived mice with respect to the size of their perfuseable worm burdens, a marginal reduction in the number of eggs deposited in the tissues and a marked reduction in the rate of egg excretion was observed in the latter animals relative to the immunologically intact controls. Treatment of S. mansoni-infected, T-cell deprived mice with serum obtained from chronically infected, immunologically intact mice prolonged their survival and reduced serum transaminase concentrations. Serum from a rabbit that had been injected with S. mansoni egg homogenate also reduced serum transaminase concentrations of infected deprived mice. The polymorphonuclearcytosis associated with S. mansoni infections in deprived mice was not affected by administration of chronic infection serum. The respective contributions of cell-mediated and humoral immune mechanisms to the protection of host tissues against the toxic effects of S. mansoni egg products are discussed.

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