Egg laying is delayed but worm fecundity is normal in SCID mice infected with Schistosoma japonicum and S-mansoni with or without recombinant tumor necrosis factor alpha treatment

Mice with severe combined immunodeficiency (SCID mice) lack functional B an d T cells. Egg laying by Schistosoma mansoni and S. japonicum was delayed i n SCID mice, but in a matter of weeks worm fecundity was equivalent to that in intact mice. SCID mice formed smaller hepatic granulomas and showed les s fibrosis than did intact mice, The reduction in egg-associated pathology in SCID mice correlated with marked reductions in interleukin-4 (IL-4), IL- 5, IL-13, and gamma interferon mRNA expression in the liver. S, mansoni inf ections were frequently lethal for SCID mice infected for more than 9 weeks , while S. japonicum-infected SCID mice died at the same rate as infected i ntact mice. We were unable to affect hepatic granuloma formation or egg lay ing by worms in SCID mice by administration of recombinant murine tumor nec rosis factor alpha (TNF-alpha). In fact, SCID and BALB/c mice appeared to e xpress nearly equivalent levels of TNF-alpha mRNA in their granulomatous ti ssues, suggesting that there is little or no deficit in TNF-alpha expressio n in infected SCID mice. The data indicate that TNF-alpha may be in large p art derived from a non-T-cell source. Together, these findings provide litt le evidence that TNF-alpha alone can reconstitute early fecundity, granulom a formation, or hepatic fibrosis in schistosome-infected SCID mice.