Induction of eotaxin expression and release from human airway smooth muscle cells by IL-1β and TNFα:: effects of IL-10 and corticosteroids
Induction of eotaxin expression and release from human airway smooth muscle cells by IL-1β and TNFα:: effects of IL-10 and corticosteroids
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DOI：
10.1038/sj.bjp.0702660
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发表时间：
1999-07-01
影响因子：
7.3
通讯作者：
Belvisi, M
中科院分区：
文献类型：
--
作者：
Chung, KF;Patel, HJ;Belvisi, M
1 Eotaxin is a novel C-C chemokine with selective chemoattractant activity for eosinophiis. 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.2 Stimulation of the cells with interleukin-1 beta (IL-1 beta) or tumour necrosis factor (TNF alpha) each at 10 ng ml(-1) induced the release of eotaxin protein with maximal accumulation by 24 h. Interferon-gamma (IFN gamma) alone at 10 ng ml(-1) had no effect and there was no synergy between these cytokines on the release of eotaxin.3 Reverse phase high performance liquid chromatographic (HPLC) analysis of supernatents from cells treated with TNF alpha (10 ng ml(-1)) for 96 h showed immunoreactivity to eotaxin which eluted with the expected retention time of 34.5-35 min.4 Both IL-1 beta and TNF alpha-induced release of eotaxin was not inhibited by dexamethasone (1 mu 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-1 beta or TNF alpha.5 Thus, human airway smooth muscle cells can release eotaxin and could be an important source of chemokine production during airway inflammatory events.
