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Background: A major allergen from the lymphatic filarial parasite Brugia malayi implicated in the pathogenesis of trop- ical pulmonary eosinophilia (TPE) has recently been cloned and identified as the homolog of the membrane-bound mammalian enzyme  -glutamyl transpeptidase ( -GT). Pa- tients with acute TPE show autoreactive antibodies against endogenous  -GT from the pulmonary epithelium. Materials and Methods: Recombinant B. malayi  -GT, alone or adsorbed to aluminium hydroxide (AL), was used in a BALB/c mouse model to analyze its antigenic/allergenic potential, its potential to induce pulmonary inflammation, and its capacity to induce autoreacting antibodies. Results: Mice immunized with B. malayi  -GT showed significant levels of  -GT-specific IgG1, IgG2a, IgG3, IgA, IgE antibodies, and mild blood eosinophilia, even in the absence of adjuvant. Intranasal challenge with B. malayi  -GT induced peribronchial and perivascular inflammation characterized by a mixed infiltrate of lymphocytes, neu- trophils, eosinophils, and macrophages. Both IL-4 and IFN- were detected in the peripheral blood and in the bronchoalveolar lavage fluid of immunized and intranasally challenged mice. Histological analysis of murine lungs us- ing affinity-purified antibodies from mice immunized with the parasite's  -GT revealed the presence of autoimmune an- tibodies against pulmonary epithelium. Western blot analy- sis identified the 55 kDa heavy chain subunit of the murine  -GT as the target of autoreactive / crossreacting antibodies. Conclusion: Our data from the in vivo mouse model demonstrate the potent allergenicity/antigenicity of B. malayi  -GT, and its capacity to induce pulmonary inflammation upon intranasal challenge. This leads to breakdown of tol- erance against endogenous murine  -GT. Thus, humoral autoimmunity against the airways epithelium may con- tribute to the pathogenesis of TPE.

Pulmonary Inflammation Induced by a Recombinant Brugia malayi γ-glutamyl transpeptidase Homolog: Involvement of Humoral Autoimmune Responses