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Published online before print February 6, 2008
Eur Respir J 2008, doi:10.1183/09031936.00121406
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ORIGINAL ARTICLE

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

C-H. Hung 1, Y-T. Chu 2, Y-M. Hua 3, S-H. Hsu 4, C-S. Lin 4, H-C. Chang 4, M-S. Lee 2, Y-J. Jong 1*

1 Dept of paediatrics, Faculty of paediatrics, College of Medicine, Kaohsiung Medical University; Dept of paediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University; and Graduate Institute of Medicine, Kaohsiung Medical University
2 Dept of paediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University
3 Dept of paediatrics, Tri-service General Hospital, Kaohsiung, Taiwan, R.O.C.
4 Graduate Institute of Medicine, Kaohsiung Medical University

* To whom correspondence should be addressed. E-mail: pedhung{at}kmu.edu.tw.


  Abstract

It is not known whether formoterol and salmeterol, two long-acting {beta}2-adrenoreceptor agonists (LABAs), have regulatory functions in Th2- and Th1- related chemokines in monocytes and bronchial epithelial cells.

We investigated the effects of two LABAs on lipopolysaccharide (LPS)-induced expression of Th2-related chemokines, MDC/CCL22, and Th1-related chemokines, IP-10/CXCL10, in a monocytic cell line, THP-1, and human primary monocytes; also, their effects on Th2-related chemokines, TARC/CCL17 expression, in an epithelial cell line, BEAS-2B, was evaluated.

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 beta2-adrenoreceptor-selective antagonist, ICI-118551. Formoterol- and LPS-induced MDC expression was inhibited by budesonide.

Both LABAs suppressed TARC expression in bronchial epithelial cells mediated via beta2-adrenoreceptors. Formoterol at physiologic concentration could suppress LPS-induced Th1-related (IP-10) but enhance Th2-related (MDC) chemokine expression in human monocytes. LABAs may increase Th2-related chemokine expression in monocytes and the Th2 cell recruitment, and, therefore, LABA monotherapy may not be an appropriate therapeutic option for asthma.

Keywords:  Bronchial epithelial cells, bronchodilators, CCL chemokines, monocyte/macrophage, {beta}2 agonist




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