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• W2889669540 abstract "BackgroundEosinophils are a therapeutic target in asthmatic patients, and GM-CSF has been suggested to control various aspects of eosinophil biology, including development, function, and survival. However, to date, the role of GM-CSF signaling in eosinophils in vivo is largely unclear.ObjectiveWe sought to elucidate the role of GM-CSF signaling in asthmatic inflammation.MethodsWild-type and GM-CSF receptor α (Csf2ra)–deficient mice reconstituted with Csf2ra-proficient alveolar macrophages were subjected to different models of airway inflammation to evaluate the effect of GM-CSF signaling deficiency on asthmatic inflammation in general and on eosinophils in particular.ResultsWe demonstrate that GM-CSF signaling, although being largely dispensable for eosinophil development at steady state, intrinsically promotes accumulation of eosinophils in the lung during allergic airway inflammation. In contrast, chitin-induced eosinophil accumulation in the peritoneal cavity occurs independent of GM-CSF, indicating organ specificity. We show that GM-CSF induces chemokinesis and promotes eosinophil survival in vitro, which likely contribute to eosinophil accumulation in the airways in vivo.ConclusionGM-CSF intrinsically promotes eosinophil accumulation in the setting of pulmonary allergic inflammation. Eosinophils are a therapeutic target in asthmatic patients, and GM-CSF has been suggested to control various aspects of eosinophil biology, including development, function, and survival. However, to date, the role of GM-CSF signaling in eosinophils in vivo is largely unclear. We sought to elucidate the role of GM-CSF signaling in asthmatic inflammation. Wild-type and GM-CSF receptor α (Csf2ra)–deficient mice reconstituted with Csf2ra-proficient alveolar macrophages were subjected to different models of airway inflammation to evaluate the effect of GM-CSF signaling deficiency on asthmatic inflammation in general and on eosinophils in particular. We demonstrate that GM-CSF signaling, although being largely dispensable for eosinophil development at steady state, intrinsically promotes accumulation of eosinophils in the lung during allergic airway inflammation. In contrast, chitin-induced eosinophil accumulation in the peritoneal cavity occurs independent of GM-CSF, indicating organ specificity. We show that GM-CSF induces chemokinesis and promotes eosinophil survival in vitro, which likely contribute to eosinophil accumulation in the airways in vivo. GM-CSF intrinsically promotes eosinophil accumulation in the setting of pulmonary allergic inflammation." @default.
• W2889669540 created "2018-09-27" @default.
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• W2889669540 date "2019-04-01" @default.
• W2889669540 modified "2023-10-14" @default.
• W2889669540 title "GM-CSF intrinsically controls eosinophil accumulation in the setting of allergic airway inflammation" @default.
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• W2889669540 doi "https://doi.org/10.1016/j.jaci.2018.08.044" @default.
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