Eosinophils are not required to induce airway hyperresponsiveness after nematode infection.

Eosinophilic inflammation of the airways is believed to play a central role in the pathogenesis of bronchial asthma. Inoculation of mice with the nematode Nippostrongylus brasiliensis induces pulmonary inflammation, characterized by a marked infiltration of eosinophils, subsequent to the migration of parasites through the lungs. Infection is associated with polarized Th2 responses in different strains of mice tested. Thus, this model may be useful to determine the relationship between established pulmonary eosinophilic inflammation, Th2 immune responses and airway changes in a nonallergic background. In the present study, we have used IL-5-deficient mice to evaluate the role of IL-5 in eosinophilic lung inflammation and airway hyperresponsiveness (AHR). In wild-type C57B/6 mice, infection with N. brasiliensis resulted in eosinophil accumulation, associated with extensive lung damage characterized by hemorrhage and alveolar wall destruction, and a strong AHR following methacholine treatment. In IL-5-deficient mice, eosinophil infiltration and the associated lung damage was abrogated. Nonetheless, AHR was unimpaired. Our results suggest that eosinophil accumulation plays a central role in lung damage but is not responsible for the induction of airway constriction following N. brasiliensis infection.