GM-CSF intrinsically controls eosinophil accumulation in allergic airway inflammation

Publication date: Available online 20 September 2018

Source: Journal of Allergy and Clinical Immunology

Author(s): Samuel Philip Nobs, Merve Kayhan, Manfred Kopf

Abstract

Background

Eosinophils are a therapeutic target in asthma 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 wild-type alveolar macrophage-reconstituted GM-CSF receptor α (Csf2ra)-deficient mice were subjected to different models of airway inflammation to evaluate the impact of GM-CSF signaling deficiency on asthmatic inflammation in general and on eosinophils in particular

Results

We demonstrate that GM-CSF signaling, while being largely dispensable for eosinophil development in steady-state, intrinsically promotes the 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 is a lung-specific regulator of eosinophil biology in pulmonary allergic inflammation.

Graphical abstract

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