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首页> 外文期刊>Mediators of inflammation >Erythromycin Enhances CD4+Foxp3+ Regulatory T-Cell Responses in a Rat Model of Smoke-Induced Lung Inflammation
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Erythromycin Enhances CD4+Foxp3+ Regulatory T-Cell Responses in a Rat Model of Smoke-Induced Lung Inflammation

机译：红霉素增强CD4 + Foxp3 +调节T细胞反应在烟雾诱导的肺炎的大鼠模型中

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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-a 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-a 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. Chronic obstructive pulmonary disease (COPD) is one of the most prevalent illnesses worldwide and is estimated as the third leading cause of mortality in 2020. COPD is characterised by airflow limitation that is poorly reversible. The pathogenesis of COPD is usually progressive and associated with an abnormal inflammatory response in the lungs, particularly in response to noxious particles or gases, such as cigarette smoke. Recently, COPD-associated inflammation is thought to be an autoimmune response induced by smoking or pathogenic microbials that activate lymphocytes and antigen-presenting cells.
机译：沉重的吸烟可以诱导气道炎症和肺气肿。大环内德可以调节肺部中的炎症和效应T细胞应答。然而，没有关于红霉素是否可以调节调节性T细胞（Treg）反应的信息。该研究旨在检查红霉素对吸烟诱导的肺气肿大鼠肺部Tregs反应的影响。每天暴露雄性Wistar大鼠每天暴露于正常空气或香烟吸烟12周，并在第四周开始每天用100mg / kg红霉素或盐水治疗。肺部炎症和支气管肺泡灌洗液（BALF）的炎症浸润的数量的特征在于。通过流式细胞术，RT-PCR和ELISA测定肺和IL-8，IL-35和TNF-A中的频率，Tregs和FoxP3表达的水平和TNF-A的水平。用红霉素治疗减少吸烟诱导的炎症浸润，BALF和肺部损伤的IL-8和TNF-A水平，但增加了CD4 + Foxp3 + Tregs的数量和肺中的Foxp3转录水平，伴随着增加的水平IL-35在大鼠Balf中。我们的新数据表明，红霉素增强的Treg反应，与抑制大鼠肺中的吸烟诱导的炎症相关。慢性阻塞性肺病（COPD）是全球最普遍的疾病之一，估计是2020年的第三次死亡原因。COPD的特点是气流限制，这是不可逆转的空气流量。 COPD的发病机制通常是渐进性的，并且与肺中的异常炎症反应相关，特别是响应有毒颗粒或气体，例如香烟烟雾。最近，认为COPD相关的炎症被认为是通过吸烟或致病微生物诱导的自身免疫应答，其激活淋巴细胞和抗原呈递细胞。

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