Circulating eosinophil/basophil progenitors and nasal mucosal cytokines inseasonal allergic rhinitis.

Accumulation of eosinophils in the airways is characteristic of allergic rh initis and asthma. The tissue eosinophilia may involve both recruitment of mature eosinophils and proliferation of their progenitors. This study exami nes mature eosinophils (nasal and circulating), their circulating progenito rs, and a potential role of granulocyte-macrophage colony-stimulating facto r (GM-CSF) in stimulating these progenitors. Twelve subjects with a history of seasonal allergic rhinitis and positive skin prick test for birch polle n were studied during four periods: shortly before, in the early and intens e phase, at the end, and well after the Swedish birch-pollen season. Nasal mucosal and circulating eosinophils were examined in both nasal brushings a nd peripheral blood samples. Eosinophil/ basophil progenitors were determin ed by counting colony-forming units in nonadherent mononuclear blood-cell c ultures in methylcellulose at 14 days. The nasal mucosal cytokines GM-CSF, interleukin (II)-1 beta, IL-3, IL-5, IL-6, IL-8, and RANTES were analyzed ( ELISA) in nasal ravage (NAL) fluids. All patients developed severe symptoms of rhinitis at the height of the season, with increased numbers of eosinop hils in the nasal mucosa (P<0.05) and in the circulation (P<0.05). At this time point, the number of circulating progenitors (P<0.05) and the NAL flui d level of CM-CSF (P<0.05) were also increased. In contrast, there was no c hange in the NAL fluid levels of IL-1 beta, IL-3, IL-6, or IL-8. Neither IL -5 nor RANTES could be detected in any of the NAL fluids. At the end of or after the season, there was no increase in nasal eosinophils or circulating eosinophils or progenitors (P>0.05). Ex vivo addition of GM-CSF (10-100 U) increased the number of blood progenitors grown before (P<0.01) and after (P<0.05) the season, compared with during the season. The in vitro GM-CSF r esponsiveness of progenitors may be related to whether or not these already have been stimulated endogenously by GM-CSF. Taken together, our data thus suggest that GM-CSF may play a role in vivo to increase production of eosi nophilic progenitors in allergic airway disease.