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Infection and Immunity, May 2003, p. 2462-2467, Vol. 71, No. 5
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.5.2462-2467.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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

Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut 06030-3105

Received 2 December 2002/ Returned for modification 9 January 2003/ Accepted 30 January 2003

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.

Editor: W. A. Petri, Jr.