Eosinophil-degranulation products drive a proinflammatory fibroblast phenotype

Eosinophils contribute to asthma pathobiology by releasing granule proteins and additional factors including cytokines and chemokines that can activate other cell types, such as bronchial fibroblasts.3,4 Although bronchial fibroblasts contribute to airway remodeling in asthma by depositing extracell...

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Bibliographic Details
Published in:Journal of allergy and clinical immunology 2018-10, Vol.142 (4), p.1360-1363.e3
Main Authors: Bernau, Ksenija, Leet, Jonathan P., Esnault, Stephane, Noll, Andrea L., Evans, Michael D., Jarjour, Nizar N., Sandbo, Nathan
Format: Article
Language:English
Subjects:
Allergies
Asthma
Cell culture
Chemokines
Cloning
Degranulation
Fibroblasts
Gene expression
Inflammation
Leukocytes (eosinophilic)
Life Sciences
Ligands
Neutrophils
Phenotypes
Proteins
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Summary:Eosinophils contribute to asthma pathobiology by releasing granule proteins and additional factors including cytokines and chemokines that can activate other cell types, such as bronchial fibroblasts.3,4 Although bronchial fibroblasts contribute to airway remodeling in asthma by depositing extracellular matrix proteins, their interactions with eosinophils are not well characterized.4 We recently performed RNA sequencing on parenchymal lung fibroblasts stimulated with activated-eosinophil–conditioned media.5 Pathway analysis revealed a gene expression profile enriched in genes involved in neutrophil recruitment and activation.5 In the present study, we sought to expand on these investigations using ex vivo cell culture models relevant to asthma pathogenesis. Eosinophil medium alone, medium with 1 ng/mL IL-3 and 0.5 μg/mL HAIgG (recombinant human IL-3 plus soluble HAIgG), and ESs from IL-3–treated eosinophils (IL-3 ESs) were used as controls.5 After 24 hours of incubation, we observed a significant increase in the expression of 4 proneutrophilic genes, chemokine (C-X-C motif) ligand 8, IL6, chemokine (C-X-C motif) ligand 1, and intercellular adhesion molecule 1 by quantitative PCR in HBFs treated with IL-3-HAIgG ES, compared with controls (Fig 1, A-D).5,8 This was consistent with our previous findings in parenchymal lung fibroblasts.5 We then assessed HBF secretion of the proneutrophilic chemokines IL-8 and IL-6 after 72 hours by ELISA. [...]we sought to determine whether HBF-conditioned media would modify neutrophil chemotaxis. [...]using an ex vivo model of eosinophil degranulation, we have found that HBFs release IL-6 and IL-8, and promote neutrophil migration.
ISSN:0091-6749
1097-6825
DOI:10.1016/j.jaci.2018.05.037