LAUSR

Repeated inhalation of airborne conidia derived from the fungus Aspergillus fumigatus (Af) can lead to a severe eosinophil‐dominated inflammatory condition of the lung termed allergic bronchopulmonary aspergillosis (ABPA). ABPA affects about 5 million individuals worldwide and the mechanisms regulating lung pathology in ABPA are poorly understood. Here, we used a mouse model of ABPA to investigate the role of eosinophils and T cell‐derived IL‐4/IL‐13 for induction of allergic lung inflammation. Selective deletion of IL‐4/IL‐13 in T cells blunted the Af‐induced lung eosinophilia and further resulted in lower expression of STAT6‐regulated chemokines and effector proteins such as Arginase 1, Relm‐α, Relm‐β, and Muc5a/c. Eosinophil‐deficient ΔdblGata mice showed lower IL‐4 expression in the lung and the number of Th2 cells in the lung parenchyma was reduced. However, expression of the goblet cell markers Clca1 and Muc5a/c, abundance of mucin‐positive cells, as well as weight gain of lungs were comparable between Af‐challenged ΔdblGata and WT mice. Based on these results, we conclude that T cell‐derived IL‐4/IL‐13 is essential for Af‐induced lung eosinophilia and inflammation while eosinophils may play a more subtle immunomodulatory role and should not simply be regarded as pro‐inflammatory effector cells in ABPA.