Erythromycin enhances CD4+Foxp3+ regulatory T-cell responses in a rat model of smoke-induced lung inflammation.
Erythromycin enhances CD4+Foxp3+ regulatory T-cell responses in a rat model of smoke-induced lung inflammation.
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DOI：
10.1155/2012/410232
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发表时间：
2012
影响因子：
4.6
通讯作者：
Deng JM
中科院分区：
文献类型：
--
作者：
Bai J;Qiu SL;Zhong XN;Huang QP;He ZY;Zhang JQ;Liu GN;Li MH;Deng JM
大量吸烟可诱发气道炎症和肺气肿。大环内酯类可调节肺部炎症和效应T细胞反应。然而，没有关于红霉素是否可以调节调节性T细胞（Treg）应答的信息。本研究旨在检查红霉素对吸烟诱导的肺气肿大鼠模型中肺中Treg应答的影响。雄性Wistar大鼠每天暴露于正常空气或吸烟12周，并从第四周开始每天用100 mg/kg红霉素或盐水灌胃治疗9周。观察肺组织炎症反应及支气管肺泡灌洗液（BALF）中炎性细胞浸润情况。采用流式细胞术、RT-PCR和ELISA法分别检测肺组织中T淋巴细胞数量、Foxp 3表达和BALF中IL-8、IL-35和TNF-α水平。红霉素治疗可减轻吸烟引起的炎症浸润，降低BALF中IL-8和TNF-α的水平，减轻肺损伤，但可增加肺中CD 4 + Foxp 3 + T淋巴细胞数量和Foxp 3转录水平，同时增加BALF中IL-35的水平。我们的新数据表明，红霉素增强Treg反应，与抑制吸烟诱导的大鼠肺部炎症有关。
Heavy smoking can induce airway inflammation and emphysema. Macrolides can modulate inflammation and effector T-cell response in the lungs. However, there is no information on whether erythromycin can modulate regulatory T-cell (Treg) response. This study is aimed at examining the impact of erythromycin on Treg response in the lungs in a rat model of smoking-induced emphysema. Male Wistar rats were exposed to normal air or cigarette smoking daily for 12 weeks and treated by gavage with 100 mg/kg of erythromycin or saline daily beginning at the forth week for nine weeks. The lung inflammation and the numbers of inflammatory infiltrates in bronchoalveolar lavage fluid (BALF) were characterized. The frequency, the number of Tregs, and the levels of Foxp3 expression in the lungs and IL-8, IL-35, and TNF-α in BALF were determined by flow cytometry, RT-PCR and ELISA, respectively. Treatment with erythromycin reduced smoking-induced inflammatory infiltrates, the levels of IL-8 and TNF-α in the BALF and lung damages but increased the numbers of CD4+Foxp3+ Tregs and the levels of Foxp3 transcription in the lungs, accompanied by increased levels of IL-35 in the BALF of rats. Our novel data indicated that erythromycin enhanced Treg responses, associated with the inhibition of smoking-induced inflammation in the lungs of rats.
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影响因子：
82.9
作者：
Ait-Oufella, H;Salomon, BL;Mallat, Z
通讯作者：
Mallat, Z
影响因子：
3.7
作者：
NAGAI, H;SHISHIDO, H;KURASHIMA, A
通讯作者：
KURASHIMA, A
DOI：
10.1016/j.ijporl.2006.10.016
发表时间：
2007-02-01
影响因子：
1.5
作者：
Ishida, Yoshiya;Abe, Yusuke;Harabuchi, Yasuaki
通讯作者：
Harabuchi, Yasuaki
影响因子：
82.9
作者：
Lee, Seung-Hyo;Goswami, Sangeeta;Kheradmand, Farrah
通讯作者：
Kheradmand, Farrah
DOI：
10.1164/rccm.200707-1134oc
发表时间：
2008-01-15
影响因子：
24.7
作者：
Simpson, Jodie L.;Powell, Heather;Gibson, Peter G.
通讯作者：
Gibson, Peter G.