Bone marrow progenitors in allergic airways diseases: studies in canine and human models

In a canine model of Ascaris suum-inducible bronchial hyperresponsiveness, we previously demonstrated that bone marrow-derived myeloid progenitors rise within 24 h of allergen inhalation; this effect is abolished by pretreatment with inhaled budesonide. We now report that this allergen-induced bone marrow response is observable in human asthmatics, and involves increases in both neutrophil-macrophage and eosinophil-basophil progenitors, within 6 h of allergen inhalation, as measured either by hematopoietic colony assays or by flow cytometric analyses of CD34+, IL-3R alpha+, and/or IL-5-responsive cell populations. In dogs, but not in humans, a transferrable serum hematopoietic activity accounts for the marrow response to inhaled allergen. These findings suggest that allergen-induced increases in bone marrow progenitor formation depend either on a serum hematopoietic factor(s) released after allergen challenge, or upon constitutive marrow upregulation of specific progenitors in allergic airway disease. Further studies to characterize the serum hematopoietic factor(s) and to determine the nature of any atopy-related progenitor profile are in progress.