Rationale: Epidemiological studies suggest that infections with helminths protect from the development of asthma. Supporting this view is our published finding that infection with Nippostrongylus brasiliensis decreased ovalbumin-induced Th2 responses in the lung of mice. Objectives: To evaluate if Nippostrongylus brasiliensis excretory/secretory products also prevent the development of asthma. Methods: Mice were immunized with ovalbumin/alum intraperitoneally in the absence/presence of helminthic products and then challenged intranasally with ovalbumin. Six days later we analyzed if the mice developed Th2 responses in the lung. Main results: The application of the helminthic products together with ovalbumin/alum during the sensitization period totally inhibited the development of eosinophilia and goblet cell metaplasia in the airways and also strongly reduced the development of airway hyperreactivity. Allergen-specific IgG1 and IgE serum levels were also strongly reduced. These findings correlated with decreased levels of IL-4 and IL-5 in the airways in product-treated animals. The suppressive effects on the development of allergic responses were independent of the presence of toll-like receptor -2, -4, IFN- and most importantly IL-10. Interestingly, suppression was still observed when the helminthic products were heated or treated with proteinase K. Paradoxically, we found that strong helminth product-specific Th2 responses were induced in parallel with the inhibition of ovalbumin-specific responses. Conclusion: Our results suggests that helminths suppress the development of asthma by secreting substances, which modulate allergic responses without affecting the generation of helminth-specific Th2 immunity. The identification of these products may lead to the design of novel therapeutic intervention strategies for the treatment of asthma.