BACKGROUND: Eosinophilic airway inflammation is a characteristic feature of bronchial asthma. Recent studies showed that increased production and release of eosinophils from bone marrow(BM) might be the essential step in the development of eosinophilic airway inflammation. To testify the hypothesis that increase in BM eosinophil production may be an important determinant of the severity of airway eosinophilia, their relationship was studied in a mouse model of allergic airway inflammation. METHODS: BALB/c mice were sensitized with intraperitoneal ovalbumin adsorbed to aluminum potassium sulfate, followed by challenges with intranasal ovalbumin on two consecutive days. Saline was used for sensitization and challenge in control mice. Bronchoalveolar lavage(BAL) was performed at 24 h after last nasal challenge, immediately followed by BM cell harvest from the femurs. The severity of airway inflammation was assessed as BAL eosinophilia, and the capacity of BM eosinophil production was assessed as BM eosinophil colony forming units(Eo-CFUs) using a semisolid culture assay. RESULTS: There was a significant increase in the percentage of BAL eosinophils and lymphocytes with a resultant decrease in the percentage of alveolar macrophages in the ovalbumin- treated mice, compared with the saline-treated mice(p<0.05, respectively). Change in the percentage of neutrophils was not statistically significant. Compared with the saline-treated mice, the number of BM Eo-CFUs was significantly increased in the ovalbumin- treated mice(p<0.05). But the number of BM Eo-CFUs was not correlated significantly with the number of eosinophils in BAL fluid in the ovalbumin-treated mice. CONCLUSION: Respiratory exposure to allergen induced not only airway eosinophilia but also BM eosinophilopoiesis in this mice model of asthma. However there was no direct relationship between BM eosinophilopoiesis and airway eosinophilia, suggesting that the capacity of eosino-phil production in BM may not an important determinant of severity of airway eosinophilia.