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Induction of eotaxin expression and release from human airway smooth muscle cells by IL‐1β and TNFα: effects of IL‐10 and corticosteroids
Author(s) -
Chung K Fan,
Patel Hema J,
Fadlon Emma J,
Rousell Jonathan,
Haddad ElBdaoui,
Jose Peter J,
Mitchell Jane,
Belvisi Maria
Publication year - 1999
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0702660
Subject(s) - eotaxin , tumor necrosis factor alpha , chemokine , dexamethasone , interleukin 8 , interleukin , endocrinology , medicine , cytokine , chemistry , stimulation , immunology , pharmacology , inflammation
Eotaxin is a novel C‐C chemokine with selective chemoattractant activity for eosinophils. We determined whether eotaxin could be produced by human airway smooth muscle (HASM) cells in culture and examined its regulation by interleukin‐10 (IL‐10) and the corticosteroid, dexamethasone. Stimulation of the cells with interleukin‐1β (IL‐1β) or tumour necrosis factor (TNFα) each at 10 ng ml −1 induced the release of eotaxin protein with maximal accumulation by 24 h. Interferon‐γ (IFNγ) alone at 10 ng ml −1 had no effect and there was no synergy between these cytokines on the release of eotaxin. Reverse phase high performance liquid chromatographic (HPLC) analysis of supernatents from cells treated with TNFα (10 ng ml −1 for 96 h showed immunoreactivity to eotaxin which eluted with the expected retention time of 34.5–35 min. Both IL‐1β and TNFα‐induced release of eotaxin was not inhibited by dexamethasone (1 μ M ), however IL‐10 (10 ng ml −1 ) had a significant inhibitory effect. Dexamethasone and IL‐10 did not inhibit the induction of eotaxin mRNA induced by IL‐1β or TNFα. Thus, human airway smooth muscle cells can release eotaxin and could be an important source of chemokine production during airway inflammatory events.British Journal of Pharmacology (1999) 127 , 1145–1150; doi: 10.1038/sj.bjp.0702660