Allergic inflammation is associated with the marked infiltration of eosinophils in affected tissues. Eosinophilia, in turn, is a hallmark clinical feature associated with allergic rhinitis, atopic dermatitis, sinusitis, and asthma. There is considerable evidence in animal models and humans that the bone marrow plays an integral role in allergic inflammation. Evidence shows that, in response to allergen exposure in the airway, bone marrow (white blood cell) progenitors proliferate and differentiate, which leads to persistent increases in eosinophil numbers. These observations suggest that there is signaling between the lung and bone marrow after allergen exposure and provide further support for the proposition that allergy is a systemic disease. Although the nature of the signal-mediating activation of bone marrow after airway allergen exposure is unknown, several pathways have been implicated, including allergen-induced hemopoietic growth factors, cell trafficking, and stimulation of resident bone marrow cells. A common thread in all these pathways is the importance of IL-5. Evidence is reviewed in animal models for the role of bone marrow in allergic inflammation within the context of the systemic nature of allergic disease.