| 大气细颗粒物诱导IL-17A表达增强香烟暴露小鼠气道炎症反应的机制 |
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| 引用本文： | 钟宇,苏国媚,熊志林,黄彤,罗朝乐,赖天文. 大气细颗粒物诱导IL-17A表达增强香烟暴露小鼠气道炎症反应的机制[J]. 中华全科医学, 2021, 19(4): 542-546. DOI: 10.16766/j.cnki.issn.1674-4152.001856 |
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| 作者姓名： | 钟宇 苏国媚 熊志林 黄彤 罗朝乐 赖天文 |
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| 作者单位： | 广东医科大学附属医院呼吸与危重症医学科，广东 湛江 524001 |
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| 基金项目： | 广东省基础与应用基础研究项目(2018A0303130269;2020B1515020004)。 |
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| 摘 要： | 目的 探讨大气细颗粒物(PM)增强香烟暴露小鼠炎症反应的机制.方法 用野生型(WT)及IL-17A基因敲除(IL-17A-/-)小鼠,按随机数字表法随机分为对照组、熏烟组、PM组、熏烟+PM组,每组6～8只.采用香烟烟雾暴露装置烟熏,气道滴注方法吸入PM,观察气道炎症反应,连续干预3个月后取检.用HE检测肺组织炎症浸润...
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| 关 键 词： | 大气细颗粒物 气道炎症 白介素17A |
| 收稿时间： | 2020-09-05 |
PM-induced IL-17A expression enhances airway inflammation in cigarette-exposed mice |
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| ZHONG Yu,SU Guo-mei,XIONG Zhi-lin,HUANG Tong,LUO Chao-le,LAI Tian-wen. PM-induced IL-17A expression enhances airway inflammation in cigarette-exposed mice[J]. Applied Journal Of General Practice, 2021, 19(4): 542-546. DOI: 10.16766/j.cnki.issn.1674-4152.001856 |
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| Authors: | ZHONG Yu SU Guo-mei XIONG Zhi-lin HUANG Tong LUO Chao-le LAI Tian-wen |
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| Affiliation: | Department of Respiratory and Critical Care Medicine, the Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, China |
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| Abstract: | Objective This study aimed to investigate the mechanisms of atmospheric fine particulate matter(PM),which enhanced the inflammatory response in cigarette-exposed mice.Methods Wild-type and IL-17 A knockout(IL-17 A-/-)mice were randomly divided into the control group,smoked group,PM group and smoked+PM group according to the random number table method(6-8 mice/group).Mice were exposed to smoke using cigarette smoke exposure device.PM was inhaled by airway instillation,and airway inflammation was observed.After continuous intervention for 3 months,mice were sacrificed to measure airway inflammation.HE was used to detect inflammatory infiltration in lung tissue,and ELISA and RT-PCR were used to detect inflammatory cytokines in lung tissue.Smooth muscle expression was detected by immunohistochemistry,and collagen deposition was observed by Masson staining.In addition,IL-17 A-secreting lymphocytes were detected by cell flow cytometry.In in vitro experiments,different concentrations of cigarette smoke extract(CSE)and/or PM were used to stimulate human airway epithelial(HBE)cells,and IL-17 A siRNA was used to knock down IL-17 A gene in HBE cells.RT-PCR detects the expression of inflammatory factors.Results Compared with the control,smoked and PM groups,lung tissue inflammatory factors(CXCL1,TFG-β1,IL-6 and IL-17 A),collagen deposition and smooth muscle expression were significantly increased in the smoked+PM group.By contrast,IL-17 A-/-mice can alleviate the above-mentioned indicators.Flow cytometry found that PM promoted IL-17 A expression by regulating CD4 cells and worsened the inflammatory response induced by smoking.In vitro,CSE or PM intervention in HBE cells can induce the secretion of IL-6 and IL-8,whereas CSE combined with PM can further increase the expression of IL-6 and IL-8.Knockout of IL-17 A gene in HBE cells can alleviate the expression of IL-6 and IL-8.Conclusion PM can induce the expression of IL-17 A and exacerbate the inflammation,collagen deposition and smooth muscle hyperplasia in the lung tissue of cigarette-exposed mice,suggesting that targeted therapy for the IL-17 A signalling pathway may be effective in relieving acute exacerbation of COPD caused by PM. |
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| Keywords: | Particulate matter Airway inflammation IL-17A |
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