title: Eosinophils express functional IL-13 in eosinophilic inflammatory diseases.
abstract: IL-13 is an immunoregulatory and effector cytokine in allergic diseases such as bronchial asthma. A variety of immune and non-immune cells are known as IL-13 producers. In this study we investigated whether and under what conditions human eosinophils generate IL-13. Freshly isolated highly purified peripheral blood eosinophils from patients with several eosinophilic inflammatory diseases and from normal control individuals were investigated. We observed that blood eosinophils from patients suffering from bronchial asthma, atopic dermatitis, parasitic infections, hypereosinophilic syndrome, and idiopathic eosinophilic esophagitis expressed IL-13, as assessed by ELISA, ELISPOT assay, flow cytometry, and immunocytochemistry. By using nasal polyp tissues and immunohistochemistry, we demonstrated IL-13 expression in eosinophils under in vivo conditions. In contrast, blood eosinophils from control individuals as well as blood neutrophils from both eosinophilic and control patients did not produce detectable IL-13 levels. However, when blood eosinophils from control individuals were stimulated with GM-CSF or IL-5 in vitro, they generated IL-13 mRNA and protein, suggesting that IL-13 expression by eosinophils under inflammatory conditions is a cytokine-driven process. Stimulation of blood eosinophils containing IL-13 by eotaxin resulted in a rapid release of this cytokine. Eosinophil-derived IL-13 was functional, as it increased the surface expression of the low affinity IgE receptor (CD23) on purified B cells. In conclusion, human eosinophils are able to produce and release functional IL-13 in eosinophilic inflammatory responses.
authors.affiliation: Swiss Institute for Allergy and Asthma Research, Davos-Platz, Switzerland. peter.schmid@hin.ch
authors.forename: Peter
authors.initials: P
authors.lastname: Schmid-Grendelmeier
authors.forename: Frank
authors.initials: F
authors.lastname: Altznauer
authors.forename: Barbra
authors.initials: B
authors.lastname: Fischer
authors.forename: Christian
authors.initials: C
authors.lastname: Bizer
authors.forename: Alex
authors.initials: A
authors.lastname: Straumann
authors.forename: Günter
authors.initials: G
authors.lastname: Menz
authors.forename: Kurt
authors.initials: K
authors.lastname: Blaser
authors.forename: Brunello
authors.initials: B
authors.lastname: Wüthrich
authors.forename: Hans-Uwe
authors.initials: HU
authors.lastname: Simon
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002462:Cell Membrane / Q000276:immunology / Q000378:metabolism; D002478:Cells, Cultured; D003876:Dermatitis, Atopic / Q000276:immunology; D004802:Eosinophilia / Q000276:immunology* / Q000473:pathology*; D004804:Eosinophils / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D004941:Esophagitis / Q000276:immunology; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D017681:Hypereosinophilic Syndrome / Q000276:immunology / Q000473:pathology; D018793:Interleukin-13 / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D015848:Interleukin-5 / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism; D011657:Pulmonary Eosinophilia / Q000276:immunology / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis; D017455:Receptors, IgE / Q000096:biosynthesis
chemical_list: D018793:Interleukin-13; D015848:Interleukin-5; D012333:RNA, Messenger; D017455:Receptors, IgE; D016178:Granulocyte-Macrophage Colony-Stimulating Factor