Schistosoma mansoni infection in IgE-producing and IgE-deficient mice.

The immunoglobulin E (IgE) response, a hallmark of helminthic infection, is generally considered a major host defense against schistosomiasis mansoni. In support, it was reported that mice with a null mutation of the Ce gene, which are thus incapable of making IgE, developed Schistosoma mansoni worm burdens 2-fold greater than wild-type mice. However, in another study, reduction of the IgE response in mice to a primary S. mansoni infection by anti-IgE treatment resulted in decreased worm burden and fecundity, suggesting that IgE plays a detrimental, rather than beneficial, role for the host in schistosomiasis. In a third study, S. mansoni worm burden and egg production in normal and in IL-4-deficient mice that produce negligible IgE levels did not differ significantly, and it appeared that IgE did not affect parasite survival or fecundity. In an attempt to resolve these controversies, we examined hepatic worm load and egg production in the liver and small intestine of IgE-deficient (SJA/9) and control IgE-producing (SJL/J) mice, 8 wk after S. mansoni infection. No differences were observed in worm burden, total egg production, and number of eggs produced per female worm in the 2 mouse strains, confirming the data that imply that IgE does not play an essential role in primary S. mansoni infection.