福莫特罗与沙美特罗对支气管上皮细胞嗜酸性粒细胞趋化因子－1的抑制作用
2010/02/03
嗜酸性粒细胞趋化因子-1(CCL11)是嗜酸性粒细胞的特异性C-C 趋化因子，是一种较强效的趋化剂，受过敏刺激后，产生的CCL11能趋化嗜酸性粒细胞迁移至气道。CCL11能趋化嗜酸性粒细胞至炎症部位，对哮喘的发病起着重要作用。福莫特罗和沙美特罗是两种吸入性长效β2肾上腺素受体激动剂(LABAs)，广泛用于哮喘的局部治疗。然而，两者对支气管上皮CCL11表达的影响了解较少。对有或无福莫特罗或沙美特罗预处理的BEAS-2B 细胞给予IL-4处理。分别采用ELISA和实时PCR检测CCL-11蛋白和mRNA表达。采用western blot和免疫荧光检测福莫特罗和沙美特罗对核内和胞浆内pSTAT-6表达的影响。
结果福莫特罗和沙美特罗(10-7-10-10 m)能显著下调BEAS-2B细胞IL-4处理后的CCL11表达。特异性β2肾上腺素受体拮抗剂（ICI118,551）则能逆转福莫特罗和沙美特罗对CCL11表达的抑制作用。福司可林（cAMP活化剂）能抑制IL-4诱导的CCL11的表达，该作用呈剂量依赖性(10-7-10-10 m)。western blot和免疫荧光研究显示，福莫特罗（10-7 m）能抑制pSTAT-6的核内表达。福莫特罗和沙美特罗能下调BEAS-2B细胞在IL-4处理后的CCL11表达。这表明该作用通过β2肾上腺素受体和cAMP介导。高浓度福莫特罗能显著下调pSTAT6表达，抑制IL-4信号通路。
（苏楠 审校）
Pediatr Allergy Immunol.. [Epub ahead of print]
Suppressive effects of formoterol and salmeterol on eotaxin-1 in bronchial epithelial cells.
Chu YT, Chang TT, Jong YJ, Kuo PL, Lee HM, Lee MS, Chang HW, Hung CH.
Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Suppressive effects of formoterol and salmeterol on eotaxin-1 in bronchial epithelial cells. Pediatr Allergy Immunol 2009. (c) 2009 John Wiley & Sons A/SEotaxin-1 (CCL11), an eosinophil-specific C-C chemokine, is a potent chemoattractant for mobilization of eosinophils into airways after allergic stimulation. Eotaxin-1 recruits eosinophils into inflammatory sites, and may play a role in the pathogenesis of asthma. Formoterol and salmeterol are two inhaled long acting beta(2) adrenoceptor agonists (LABAs), widely used for the local treatment of asthma. However, little is known about their effects on the eotaxin-1 expression of bronchial epithelial cells. BEAS-2B cells were stimulated by adding IL-4 with or without 2 h pre-treatment of formoterol or salmeterol. The protein and mRNA expression of eotaxin-1 were measured by ELISA assay and real-time PCR, respectively. Effects of formoterol and salmeterol on nuclear and cytosolic pSTAT-6 expression were evaluated by Western blot and immunofluorescence study. Formoterol and salmeterol (10(-7)-10(-10) m) significantly down-regulated IL-4- induced eotaxin-1 expression in BEAS-2B cells. A specific beta(2) adrenoceptor antagonist (ICI 118,551) reversed their suppression of eotaxin-1 production. Forskolin, an cAMP activator, could also suppress the expression of eotaxin-1 by IL-4 in a dose dependent manner (10(-7)-10(-10 )m). The western blot and immunofluorescence studies demonstrated that formoterol 10(-7 )m suppressed the nuclear expression of pSTAT-6. Formoterol and salmeterol, two inhaled long-acting beta(2) agonists, down-regulated IL-4- induced eotaxin-1 expression in BEAS-2B cells. The effect was mediated via the beta(2) adrenoceptor, and cAMP. Formoterol significantly down-regulated pSTAT6 at higher concentration, and further turned off the IL-4 signaling pathway.
Pediatr Allergy Immunol.. [Epub ahead of print]
结果福莫特罗和沙美特罗(10-7-10-10 m)能显著下调BEAS-2B细胞IL-4处理后的CCL11表达。特异性β2肾上腺素受体拮抗剂（ICI118,551）则能逆转福莫特罗和沙美特罗对CCL11表达的抑制作用。福司可林（cAMP活化剂）能抑制IL-4诱导的CCL11的表达，该作用呈剂量依赖性(10-7-10-10 m)。western blot和免疫荧光研究显示，福莫特罗（10-7 m）能抑制pSTAT-6的核内表达。福莫特罗和沙美特罗能下调BEAS-2B细胞在IL-4处理后的CCL11表达。这表明该作用通过β2肾上腺素受体和cAMP介导。高浓度福莫特罗能显著下调pSTAT6表达，抑制IL-4信号通路。
（苏楠 审校）
Pediatr Allergy Immunol.. [Epub ahead of print]
Suppressive effects of formoterol and salmeterol on eotaxin-1 in bronchial epithelial cells.
Chu YT, Chang TT, Jong YJ, Kuo PL, Lee HM, Lee MS, Chang HW, Hung CH.
Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Suppressive effects of formoterol and salmeterol on eotaxin-1 in bronchial epithelial cells. Pediatr Allergy Immunol 2009. (c) 2009 John Wiley & Sons A/SEotaxin-1 (CCL11), an eosinophil-specific C-C chemokine, is a potent chemoattractant for mobilization of eosinophils into airways after allergic stimulation. Eotaxin-1 recruits eosinophils into inflammatory sites, and may play a role in the pathogenesis of asthma. Formoterol and salmeterol are two inhaled long acting beta(2) adrenoceptor agonists (LABAs), widely used for the local treatment of asthma. However, little is known about their effects on the eotaxin-1 expression of bronchial epithelial cells. BEAS-2B cells were stimulated by adding IL-4 with or without 2 h pre-treatment of formoterol or salmeterol. The protein and mRNA expression of eotaxin-1 were measured by ELISA assay and real-time PCR, respectively. Effects of formoterol and salmeterol on nuclear and cytosolic pSTAT-6 expression were evaluated by Western blot and immunofluorescence study. Formoterol and salmeterol (10(-7)-10(-10) m) significantly down-regulated IL-4- induced eotaxin-1 expression in BEAS-2B cells. A specific beta(2) adrenoceptor antagonist (ICI 118,551) reversed their suppression of eotaxin-1 production. Forskolin, an cAMP activator, could also suppress the expression of eotaxin-1 by IL-4 in a dose dependent manner (10(-7)-10(-10 )m). The western blot and immunofluorescence studies demonstrated that formoterol 10(-7 )m suppressed the nuclear expression of pSTAT-6. Formoterol and salmeterol, two inhaled long-acting beta(2) agonists, down-regulated IL-4- induced eotaxin-1 expression in BEAS-2B cells. The effect was mediated via the beta(2) adrenoceptor, and cAMP. Formoterol significantly down-regulated pSTAT6 at higher concentration, and further turned off the IL-4 signaling pathway.
Pediatr Allergy Immunol.. [Epub ahead of print]
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