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

¹ Dept of Paediatrics, Faculty of Paediatrics, College of Medicine, ² Dept of Paediatrics, Kaohsiung Medical University Hospital, and ³ Graduate Institute of Medicine, Kaohsiung Medical University, and ⁴ Dept of Paediatrics, Tri-Service General Hospital, Kaohsiung, Taiwan, Republic of China.

CORRESPONDENCE: Y-J. Jong, Dept of Paediatrics, Kaohsiung Medical University Hospital, No. 100, Tz-You 1st Road, Kaohsiung 807, Taiwan, Republic of China. Fax: 886 73213931. E-mail: pedhung{at}kmu.edu.tw

Keywords: β₂-Adrenoreceptor agonist, bronchial epithelial cells, bronchodilators, CC chemokines, macrophage, monocyte

Received: September 15, 2006
Accepted January 27, 2008

It is unknown whether formoterol and salmeterol, two long-acting β₂-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--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 LPS. 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 β₂-adrenoreceptor antagonist, ICI-118551. Formoterol- and LPS-induced MDC expression was inhibited by budesonide.

Both long-acting β₂-adrenoreceptor agonists suppressed thymus- and activation-regulated chemokine expression in bronchial epithelial cells mediated via β₂-adrenoreceptors. Formoterol at physiological concentrations could suppress lipopolysaccharide-induced T-helper cell type 1-related chemokine (interferon--inducible protein-10) but enhance T-helper cell type 2-related chemokine (macrophage-derived chemokine) expression in human monocytes. Long-acting β₂-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 β₂-adrenoreceptor agonist monotherapy may not be an appropriate therapeutic option for asthma.

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