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Prolonged Eosinophil Production after Allergen Exposure in IFN‐γR KO Mice is IL‐5 Dependent

Asthma is a T helper 2 (Th2)‐driven inflammatory process characterized by eosinophilia. Prolonged airway eosinophilia is commonly observed in asthma exacerbations. Our aim was to evaluate whether eosinophilia in prolonged allergic inflammation is associated with a continuous supply of new eosinophils to the airways, and how this is regulated. Ovalbumin (OVA)‐sensitized interferon‐γ receptor knockout mice (IFN‐γR KO), known to maintain a long‐lasting eosinophilia after allergen exposure, were compared to wild type (wt) controls. Animals were exposed to OVA or phosphate‐buffered saline on three consecutive days, and bone marrow (BM), blood and bronchoalveolar lavage (BAL) samples were collected 24 h, 7 and 21 days later. Newly produced cells were labelled using bromodeoxyuridine (BrdU). Serum IL‐5 was measured and its role was investigated by administration of a neutralizing anti‐IL‐5 antibody. In‐vitro eosinophilopoiesis was examined in both groups by a colony‐forming assay. Allergen challenge increased eosinophils in BM, blood and BAL, in both IFN‐γR KO and wt mice, both 24 h and 7 days after the last allergen exposure. At 21 days after the last exposure, only IFN‐γR KO mice maintained significantly increased eosinophil numbers. Approximately 50% of BAL granulocytes in IFN‐γR KO were produced during the last 6 days. Interleukin (IL)‐5 concentration was increased in IFN‐γR KO mice, and anti‐IL‐5 reduced eosinophil numbers in all compartments. Increased numbers of eosinophil colonies were observed in IFN‐γR KO mice after allergen exposure versus controls. In this model of a Th2‐driven prolonged allergic eosinophilia, new eosinophils contribute to the extended inflammation in the airways by enhanced BM eosinophilopoiesis in an IL‐5‐dependent manner.