期刊
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 143, 期 4, 页码 1513-+出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2018.08.044
关键词
Eosinophils; asthma; allergic airway inflammation; GM-CSF; chemokinesis
资金
- Swiss National Science Foundation (SNCF) Grant [310030_163443]
- Swiss National Science Foundation (SNF) [310030_163443] Funding Source: Swiss National Science Foundation (SNF)
Background: 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. Objective: We sought to elucidate the role of GM-CSF signaling in asthmatic inflammation. Methods: Wild-type and GM-CSF receptor a (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. Results: 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. Conclusion: GM-CSF intrinsically promotes eosinophil accumulation in the setting of pulmonary allergic inflammation.
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