Haemopoietic mechanisms in nasal polyposis and asthma.

Recent studies of the involvement of the bone marrow in human atopic asthmatic responses to inhaled allergen confirm what we have found in a canine model of Ascaris suum induced bronchial hyperresponsiveness: CD34/45+ haemopoietic progenitors, increased in numbers in the blood and marrow of atopic individuals, can be specifically upregulated following airway allergen challenge eliciting bronchial hyperresponsiveness and the late phase response. These progenitors are also found in nasal polyps and in asthmatic bronchial mucosa. An interleukin (IL)-5 responsive subset of progenitors, marking the Eo-B lineage specifically, is upregulated in the marrow within 24 hours of allergen challenge in dual responder asthmatics; using triple colour flow cytometry it can be shown that this subpopulation of progenitors in the marrow is one that bears high aYnity receptors for IL-5 (IL-5Rá), existing as a subpopulation of early progenitors bearing CD34/45. 4 Thus, a readily mobilisable pool of autocrine (GM-CSF and IL-5 producing) Eo-B progenitors at a very early stage of lineage commitment is increased after inhalation of allergen only in those individuals who develop ongoing inflammatory responses. The nature of the signalling between the airway and the bone marrow, which upregulates IL-5Rá on CD34+ progenitors in the bone marrow in vivo, has not been fully clarified. We therefore undertook studies to explore the in vitro regulation of IL-5R expression on haemopoietic progenitors.