Mice Genetically Deficient in Immunoglobulin E Are More Permissive Hosts than Wild-Type Mice to a Primary, but Not Secondary, Infection with the Filarial Nematode Brugia malayi

Abstract

Primary and secondary murine and human infections with Brugia malayi are characterized by substantial increases in levels of immunoglobulin E (IgE). To investigate whether this is necessary for worm clearance, IgE −/− mice were subjected to primary- and secondary-infection protocols. Following a primary infection, IgE −/− mice displayed a profound deficit in their ability to clear an intraperitoneal injection of L3 infective-stage larvae in comparison to wild-type counterparts and maintained substantial worm burdens as late as 10 weeks postinfection. Although viable adult parasites were recovered at this late time point from IgE −/− mice, the majority of the mice remained free of microfilariae. IgE −/− cohorts subjected to a secondary-infection protocol were able to clear the challenge inoculation in an accelerated manner, with kinetics similar to that observed in the wild-type animals. Analysis of the humoral response in IgE −/− mice following infection demonstrates a defect in IgG1 and IgG2a production, in addition to the expected lack of IgE. The IgG1 deficiency is no longer evident following a secondary infection. These data imply that deficiencies other than IgE production (i.e., IgG1 production) deficiency may be responsible for the increased permissiveness of IgE −/− mice as hosts following infection with B. malayi .