Prolonged existence of helminth parasites in their mammalian hosts has led to the establishment of a very particular immunological microenvironment that supports the fitness of both the pathogen and the host. The modern way of living in developed societies has interrupted this tight relationship by almost completely removing helminths from the human population. It is believed that, as a consequence of this process, a rapid increase in the incidence of asthma and other inflammatory disorders has occurred. Data derived from experimental models clearly show that worms and their products can ameliorate asthma-like disease in mice. This review will concentrate on the effects of helminth-driven regulatory mechanisms on the function of eosinophils and neutrophils in experimental asthma. Eosinophils and neutrophils are major effector cells driving pathology in the lung, therefore learning how to control their exacerbated activation in asthma might aid in creating much needed novel therapeutics to combat this common inflammatory disorder.