Schistosoma mansoni Infection in IgE-Producing and IgE-Deficient Mice

Abstract

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.

Experimental Angiostrongylus costaricensis infection in mice: immunoglobulin isotype responses and parasite-specific antigen recognition after primary low-dose infection

“…However, no such eect was observed when IgE-de®cient SJA/9 or SJL/J wild-type mice were infected with A. costaricensis (Watanabe et al 1993). Another study, where IgE-de®cient and IgE-producing mice were infected with S. mansoni, likewise implies that IgE does not play an essential role in primary S. mansoni infection, thus further heating up this controversy (El Ridi et al 1998). …”

Experimental models of Schistosoma mansoni infection

“…treatment with anti-IgE, has been reported to inhibit the development of S. mansoni suggesting that the worms need this immunoglobulin for normal development (Amiri et al 1994). This is difficult to reconcile with the increased numbers of worms developing in IgE ko mice ) and the normal development of worms in FcεRI ko mice, in B cell ko mice and in SJA/9 mice unable to produce IgE , El Ridi et al 1998.…”

Schistosomiasis in the People's Republic of China: Prospects and Challenges for the 21st Century

“…However, IgE does not appear to play an essential role in the murine response to schistosome infection (56), as appears to be the case in the rat model and probably in humans (see below). Other work has demonstrated that protection in mice multiply vaccinated with attenuated cercariae can be mediated by humoral factors transferable in serum to naive recipients (125) and that an increased level of protection is transferable by increasing the number of vaccinations (54).…”