Open AccessComparative analysis of cytokine release from epithelial cell cultures of the upper airway
Author(s) -
Akihito Shiozawa,
Masato Miwa,
Noritsugu Ono,
H Homma,
Mikio Hirotsu,
Katsuhisa Ikeda
Publication year - 2015
Publication title -
rhinology (amsterdam. online)/rhinology
Language(s) - English
Resource type - Journals
eISSN - 1996-8604
pISSN - 0300-0729
DOI - 10.4193/rhino14.078
Subject(s) - thymic stromal lymphopoietin , medicine , nasal polyps , chemokine , cytokine , tumor necrosis factor alpha , secretion , immunology , stimulation , cxcl1 , granulocyte macrophage colony stimulating factor , proinflammatory cytokine , immune system , inflammation
Upper airway epithelial cells show a multi-potential ability to produce a variety of cytokines/chemokines in the steady-state and under external stimuli. Objective: To compare various cytokines/chemokines released from primary cultures of human nasal epithelial cells (HNECs) derived from healthy controls and subjects with allergic rhinitis (AR), chronic rhinosinusitis with nasal polyps (CRSwNPs) in non- stimulated and IL-17A-stimulated conditions. Methods: The supernatants derived from HNECs of healthy control, AR, CRSwNPs were used to measure 20 of cytokines/chemo- kines in the non-stimulated and IL-17A-stimulated conditions. Results: AR and CRSwNPs showed significant up-regulation in the release of IL-6, IL-33, and thymic stromal lymphopoietin (TSLP), and the release of IL-6, TSLP, granulocyte macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor α (TNFα) in comparison with normal controls, respectively. Secretion of GM-CSF and TNFα were enhanced in patients with nasal polyps as compared with AR. Stimulation with IL-17A enhanced the secretion of IL-8 and granulocyte-colony stimulating factor (G-CSF) in the normal control, IL-6 and IL-8 in AR, and IL-6, TSLP, G-CSF, GM-CSF and TNFα in nasal polyps. Conclusion: Epithelial cells derived from AR and CRSwNPs showed up-regulation of secretion of several cytokines/chemokines both in the steady state and after IL-17A stimulation, which may contribute to the inflammatory responses of AR and CRSwNPs.