Effects of formoterol and salmeterol on the production of Th1-and Th2-related chemokines by monocytes and bronchial epithelial cells

被引：26
作者：
Hung, C-H. [1 ,2 ]
Chu, Y-T. [1 ]
Hua, Y-M. [3 ]
Hsu, S-H. [2 ]
Lin, C-S. [2 ]
Chang, H-C. [2 ]
Lee, M-S. [1 ]
Jong, Y-J. [1 ,2 ]
机构：
[1] Kaohsiung Med Univ Hosp, Dept Paediat, Kaohsiung 807, Taiwan
[2] Kaohsiung Med Univ, Grad Inst Med, Kaohsiung, Taiwan
[3] Tri Serv Gen Hosp, Dept Paediat, Kaohsiung, Taiwan
来源：
EUROPEAN RESPIRATORY JOURNAL | 2008年 / 31卷 / 06期
关键词：
beta(2)-adrenoreceptor agonist; bronchial epithelial cells; bronchodilators; CC chemokines; macrophage; monocyte;
D O I：
10.1183/09031936.00121406
中图分类号：
R56 [呼吸系及胸部疾病];
学科分类号：
摘要：
It is unknown whether formoterol and salmeterol, two long-acting beta(2)-adrenoreceptor agonists, have regulatory functions in the production of T-helper cell (Th) type 2- and Th1-related chemokines by monocytes and bronchial epithelial cells. In the present study, the effects of formoterol and salmeterol on lipopolysaccharide (LPS)induced expression of the Th2-related chemokine macrophage-derived chemokine (MDC; CCL22) and the Th1-related chemokine interferon-gamma-inducible protein (IP)-10 (CXCL10) were investigated in a monocytic cell line, THP-1, and in human primary monocytes. In addition, their effects on the expression of the Th2-related chemokine thymus- and activation-regulated chemokine (TARC; CCL17) were evaluated in an epithelial cell line, BEAS-2B. Formoterol enhanced MDC but suppressed IP-10 production in monocytes induced by LIPS. Higher doses of salmeterol were required to enhance LPS-induced MDC expression in THP-1 cells. Formoterol and salmeterol could significantly suppress TARC expression in BEAS-2B cells. These effects could be reversed by a selective beta(2)-adrenoreceptor antagonist, ICI-118551. Formoterol- and LPS-induced MDC expression was inhibited by budesonide. Both long-acting beta(2)-adrenoreceptor agonists suppressed thymus- and activation-regulated chemokine expression in bronchial epithelial cells mediated via beta(2)-adrenoreceptors. Formoterol at physiological concentrations could suppress lipopolysaccharide-induced T-helper cell type 1-related chemokine (interferon-gamma-inducible protein-10) but enhance T-helper cell type 2-related chemokine (macrophage-derived chemokine) expression in human monocytes. Long-acting beta(2)-adrenoreceptor agonists may increase T-helper cell type 2-related chemokine expression in monocytes and T-helper cell type 2 recruitment and, therefore, long-acting beta(2)-adrenoreceptor agonist monotherapy may not be an appropriate therapeutic option for asthma.
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收藏
页码：1313 / 1321
页数：9
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