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

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 .