Pulmonary eosinophilia is a hallmark of atopic asthma and a common feature of mouse models of allergic inflammation. Different mouse strains have different sensitivity to allergens, different severity of Th2 driven inflammatory responses, and hence different degrees of induced pulmonary pathology. Indeed, many investigators have hypothesized that strain-specific differences (i.e. C57BL/6J vs. BALB/cJ) exist with regards to the utility of established allergen sensitization/challenge models. Moreover the role/contribution of eosinophils to allergen-induced pulmonary pathologies remains unresolved with suggestions that the importance of these activities may also be strain specific. We compared ovalbumin induced pulmonary allergic inflammation in eosinophil deficient mice (PHIL) on two genetic backgrounds, C57BL/6J and BALB/cJ. Lung histopathology and lung function were assessed. Our data demonstrate that the genetic ablation of eosinophils in PHIL mice occurs in both C57BL/6J vs. BALB/cJ. More importantly, irrespective of background strain the loss of eosinophils resulted in the attenuation of key allergen-induced lung pathologies. In particular, both strains of mice displayed a significant decrease in allergen-induced goblet cell metaplasia and the loss of AHR in the absence of eosinophils. Observed strain differences in terms of allergen-induced pathologies cannot be explained on the basis of strain-specific eosinophil effector functions.