Lung eosinophils elicited during allergic and acute aspergillosis express RORγt and IL-23R but do not require IL-23 for IL-17 production

Exposure to the mold, Aspergillus, is ubiquitous and generally has no adverse consequences in immunocompetent persons. However, invasive and allergic aspergillosis can develop in immunocompromised and atopic individuals, respectively. Previously, we demonstrated that mouse lung eosinophils produce IL-17 in response to stimulation by live conidia and antigens of A. fumigatus. Here, we utilized murine models of allergic and acute pulmonary aspergillosis to determine the association of IL-23, IL-23R and ROR gamma t with eosinophil IL-17 expression. Following A. fumigatus stimulation, a population of lung eosinophils expressed ROR gamma t, the master transcription factor for IL-17 regulation. Eosinophil ROR gamma t expression was demonstrated by flow cytometry, confocal microscopy, western blotting and an mCherry reporter mouse. Both nuclear and cytoplasmic localization of ROR gamma t in eosinophils were observed, although the former predominated. A population of lung eosinophils also expressed IL-23R. While expression of IL-23R was positively correlated with expression of ROR gamma t, expression of ROR gamma t and IL-17 was similar when comparing lung eosinophils from A. fumigatus-challenged wild-type and IL23p19(-/-) mice. Thus, in allergic and acute models of pulmonary aspergillosis, lung eosinophils express IL-17, ROR gamma t and IL-23R. However, IL-23 is dispensable for production of IL-17 and ROR gamma t.