Role of IgE in primary murine Schistosomiasis mansoni

Schistosoma mansoni infection proceeds in normal mice in the absence of det ectable levels of polyclonal or specific immunoglobulin (Ig)E until worms m ature and deposit eggs, Hence, the course of a primary S, mansoni infection is not expected to vary appreciably in mice with defects in the IgE produc tion. Experimental increase of IgE production early after infection may, ho wever, influence worm development. In the first approach towards this goal, BALB/c mice were injected with interleukin(IL)-4 to raise the level of end ogenously synthesized IgE, A significant increase in serum polyclonal IgE a nd antischistosome IgG1 during the prepatent period was not associated with significant changes in worm and egg burden or liver pathology. During the second approach, mice were injected with IgE which was affinity purified fr om serum of BALB/c mice infected for 16 weeks with S. mansoni. The purified IgE bound to carbohydrate-independent epitopes of soluble antigens from 3 h larvae, adult worms and eggs and recognized the schistosomular surface me mbrane, No differences in worm and egg load or granuloma number and size we re noted between untreated and exogenous IgE-injected mice. Together, the d ata demonstrate that by itself IgE does not influence the outcome of infect ion in primary murine S, mansoni.