SCHISTOSOMA-MANSONI INFECTION IN IGE-PRODUCING AND IGE-DEFICIENT MICE

The immunoglobulin E (IgE) response, a hallmark of helminthic infectio n. is generally considered a major host defense against schistosomiasi s mansoni. In support, it was reported that mice with a null mutation of the Ce gene, which are thus incapable of making IgE, developed Schi stosoma mansoni worm burdens 2-fold greater than wild-type mice. Howev er, in another study, reduction of the IgE response in mice to a prima ry S. mansoni infection by anti-IgE treatment resulted in decreased wo rm burden and fecundity, suggesting that IgE plays a detrimental, rath er than beneficial, role for the host in schistosomiasis. In a third s tudy, S. mansoni worm burden and egg production in normal and in IL-4- deficient mice that produce negligible IgE levels did not differ signi ficantly, and it appeared that IgE did nor 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 burde n, total egg production. and number of eggs produced per female worm i n the 2 mouse strains, confirming the data that imply that IgE does no t play an essential role in primary S. mansoni infection.