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双语推荐：气道重塑

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支气管哮喘(简称哮喘)是气道慢性炎症和组织改变共同参与的疾病.慢性炎症反应与气道重塑密切相关,炎症细胞和组织细胞释放多种细胞因子、趋化因子和生长因子,在气道组织里形成了复杂的信号环境促成了气道重塑.气道重塑包括一系列病理生理学特征.本文结合近年来哮喘气道重塑的文献,就病理学特点和最新机制性研究作一综述.
Bronchial asthma (asthma) is a lung disease invloved by both airway chronic inflammatory and structural alterations.Remodeling is associated with airway chronic inflammatory response.Multiple cytokines,chemokines,and growth factors released from both inflammatory and structural cells in the airway tissue form a complex signaling environment that facilitate these structural changes,which contain a wide array of pathophysiologic features.In this paper,we will make a review on pathology feathers and latest mechanism researches based on recent literatures on airway remodeling in asthma.

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支气管哮喘的气道重塑是气道炎症反复作用的结果，白三烯是气道重塑中的重要炎症介质之一。影响气道重塑的因素较多，近年来Th17细胞和CD4+CD25+调节性T细胞(CD4+CD25+treg细胞)在气道重塑中的作用日益受到重视。白三烯受体拮抗剂是治疗哮喘的有效药物，能在一定程度上抑制气道重塑，但其作用机制及对Th17细胞/CD4+CD25+treg细胞表达的影响机制尚不十分清楚。因此，阐明Th17细胞/CD4+CD25+treg细胞平衡在气道重塑中的表达变化、白三烯受体拮抗剂干预气道重塑的具体作用途径和生物效应及对Th17细胞/CD4+CD25+treg细胞表达的影响，将为以后哮喘患儿的预防和治疗提供新的靶点。
The airway remodeling of bronchial asthma is the result of repeated airway inlfammation. Its occurrence is a complex process involving many cytokines, inlfammatory mediators and associated cellular components, of which leukotrienes are important mediators of inlfammation in the airway remodeling. Many factors inlfuence Airway remodeling. In recent years, effects of Th17 cells and CD4+CD25+regulatory T cells (CD4+CD25+treg cells) on airway remodeling is growing in importance. Leukotriene receptor antagonist is an effective drug in the treatment of asthma and can suppress airway remodeling. But the exact mechanisms and its impact on the proportion of Th17 cells/CD4+CD25+treg cells is not yet clear. Therefore, the clariifcation of the changes of Th17 cells/CD4+CD25+treg cells expression in airway remodeling and the speciifc pathways, biological effects, inlfuence of the proportion of Th17 cells/CD4+CD25+treg cells expression after leukotriene receptor antagonist intervene can provide a ne

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支气管哮喘是可逆性气流受限的慢性气道炎症性疾病,气道炎症的长期存在可引起气道的重塑,但目前关于哮喘气道重塑的发病机制仍未完全阐明。近年来,许多研究发现精氨酸酶在哮喘的气道炎症和气道重塑中发挥着重要作用,其不仅能降低气道释放的NO水平,增加气道高反应性,而且其代谢产物如腐胺、脯氨酸等能诱导细胞的增殖和胶原的合成,导致气道重塑。文中就精氨酸酶及其在哮喘发病中的作用作一综述。
Bronchial asthma is the chronic airway inflammatory disease that characterized by reversible airflow limitation .The presence of airway inflammation could lead to airway remodeling .In recent years , many studies have found that arginase plays an im-portant role in the airway inflammation and airway remodeling of asthma .It not only reduces airway release nitric oxide and increases airway hyperresponsiveness , but also its metabolites such as putrescine , proline, etc can induce cell proliferation and collagen synthe-sis, leading to airway remodeling .In this paper , the arginase and its role in the pathogenesis of asthma are discussed .

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支气管哮喘(简称哮喘)气道重塑是慢性哮喘不可逆性气流受限的重要原因,是由多种细胞共同作用最终导致气道结构异常的过程,目前机制尚未完全明确.近年来,越来越多的研究结果表明,循环纤维细胞在哮喘的气道重塑中发挥着重要作用.本文就循环纤维细胞的基本生物学特性以及其参与哮喘气道重塑的研究现状及进展作一综述.
The structural remodeling of airway is an important cause of the development of progressive airflow obstruction in chronic asthma.This process is resulted from the effect of a variety of cells and leads to the abnormal structure of airways.However,the mechanism is not completely clear.In recent studies,there is increased evidence suggesting that the circulating fibrocytes play an important role in airway remodeling of asthma.This review aims to summarize the basic biological characteristics of fibrocytes and the current understanding and evidences of fibrocytes in the pathogenesis of airway remodeling in chronic asthma.

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小儿支气管哮喘（哮喘）的病理生理机制尚未完全清楚。气道重塑是其中重要的病理生理改变，参与了哮喘的发生、发展过程。解整合素-金属蛋白酶33（ADAM33）基因为哮喘的易感性基因，研究表明其与气道重塑密切相关。该文就 ADAM33在哮喘气道重塑中的作用机制进行阐述，以阐明哮喘发生的基因机制。
The pathophysiological mechanism of pediatric asthma remains elusive.Airway remodeling is part of the main pathophysiological changes which are involved in the incidence and development of asthma.A disintegrin and metalloprotease 33 (ADAM33)has been proven to be a susceptibility gene of asthma,which is closely associated with airway remodeling.This article reviewed the underlying mechanism of ADAM33 in airway remodeling in patients with asthma,and to elucidate the genetic mechanism of asthma.

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Notch信号通路参与多种组织细胞的分化、成熟过程,尤其在T淋巴细胞的分化过程中起了决定性作用。近年来,大量研究表明,Notch信号通路参与支气管哮喘(BA)发病的整个病理过程,包括气道炎症、气道高反应、气道重塑及气道血管重塑。笔者拟就Notch信号通路在BA和T淋巴细胞调节中的作用,进行综述如下。
Notch signaling pathway involves in cell differentiation process in a lot of tissues, especially playing an important role in T lymphocytes differentiation process.Recently,many reports have demonstrated that the Notch signaling pathway involves in the whole pathogenesis of bronchial asthma(BA) pathological process,including airway inflammation,airway hyperresponsiveness,airway remodeling and vascular remodeling of the airway.This paper summarizes the roles of Notch signaling pathway in BA and T lymphocyte regulation.

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目的：观察雷帕霉素对哮喘大鼠模型气道重塑和肺组织白细胞介素（IL）-8、IL-10的影响，探讨其在干预支气管哮喘气道炎症和气道重塑中的作用机制，为临床研究提供实验依据。方法建立哮喘大鼠气道重塑模型，30只SD大鼠按随机数字法随机分为正常对照组（A）、哮喘组（B）、雷帕霉素干预组（C），每组10只。对肺组织切片行苏木素-伊红染色观察气道重塑情况。采用免疫组织化学和图像分析技术的方法测定各组大鼠肺组IL-8、IL-10的表达。结果哮喘组动物出现管壁增厚、平滑肌增生、黏液分泌增加等气道重塑的特征性改变，免疫组织化学染色显示气道各层细胞及炎性细胞均有IL-8表达增多，且IL-10水平也显著减少。雷帕霉素干预组与哮喘组比较，炎症反应轻微，平滑肌增生、黏液分泌不明显，免疫组织化学染色示各细胞IL-8表达也有所降低，IL-10水平表达增高，与正常对照组比较差异有统计学意义（P＜0．05）。结论雷帕霉素可减轻哮喘大鼠的气道炎症和气道重塑，并可降低IL-8表达水平，增高IL-10表达水平，调节失衡的致炎因子/抑炎因子比例，发挥对支气管哮喘的炎症抑制和免疫调节作用。
Objective To investigate the effects of rapamycin on airway remodeling and lung tissue IL-8 and IL-10 in asthmatic rats, and to explore the mechanism by which rapamycin intervene in airway inflammation and re-modeling in bronchial asthma, so as to provide experimental basis for clinical research. Methods The asthmatic rat model of airway remodeling was established. Then, 30 SD rats were randomly divided into 3 groups: normal control group, asthma group, and rapamycin intervention group, with 10 rats in each group. Airway remodeling was observed in lung tissue sections with hematoxylin-eosin staining. The IL-8 and IL-10 expressions in lung tissues of each group were measured by immunohistochemistry and image analysis technique. Results The rats in asthma group showed characteristic changes of airway remodeling, such as thickened airway walls, hyperplasia of smooth muscle, and mucus hypersecretion. Immunohistochemical staining showed increased IL-8 expression in structural cell

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目的：研究观察多索茶碱对慢性阻塞性肺疾病患者气道重塑与痰液、血清炎性指标的影响。方法选取2011年10月～2013年8月本院收治的80例慢性阻塞性肺疾病患者为研究对象，将其随机分为对照组（氨茶碱治疗组）40例和观察组（多索茶碱治疗组）40例，两组患者治疗前与治疗后5 d、10 d的血清气道重塑指标及痰液、血清炎性指标进行检测与比较。结果观察组治疗后5 d、10 d的血清气道重塑指标及痰液、血清炎性指标均显著地低于对照组，并且观察组治疗后5 d、10 d的检测水平均明显地低于本组治疗前（P均〈0．05），均有显著性差异。结论多索茶碱可有效改善慢性阻塞性肺疾病患者气道重塑状态，并对控制痰液、血清炎性指标发挥着积极的临床作用。
Objective To study and observe the influence of doxofylline on the airway remodeling and spu-tum and serum inflammatory indexes of patients with chronic obstructive pulmonary disease. Methods 80 patients with chronic obstructive pulmonary in our hospital from October 2011 to August 2013 were randomly divided into the control group (the aminophylline treatment group) and the observation group (the doxofylline group), 40 cases in each group. The serum airway remodeling and the inflammatory indexes sputum and serum in the two groups were de-tected and compared before and 5 and 10 days after the treatment. Results 5 and 10 days after the treatment, the indexes of serum airway remodeling and sputum and serum inflammatory decreased significantly in the two groups, and the decrease was more pronounced in the observation group than in the control group (P<0. 05). Conclusion Doxofylline can effectively improve the airway remodeling state and have active clinical effect in controlling

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人软骨糖蛋白-39(YKL-40)是一种新发现的炎症因子,属于哺乳动物18-糖基水解酶家族成员.既往研究表明,YKL-40与炎症和肿瘤有关.近年来研究显示,YKL-40可能参与了支气管哮喘(简称哮喘)的发生、发展,并且与气道重塑密切相关.YKL-40的生物学功能和作用尚不完全清楚,可能均参与了哮喘的炎症反应、气道高反应性、气道重塑的过程.YKL-40对于检测哮喘患者的辅助检查、严重程度、预后判断均有一定的意义.
Human cartilage glycoprotein 39 (YKL-40) is a newly discovered inflammatory cytokine,which belongs to the member of 18 glycosyl hydrolase of mammal family.Previous studies have indicated that YKL-40 is associated with the inflammation disease and tumors.Studies in recent years have suggested that YKL-40 may be involved in the occurrence of asthma and development,and is related to airway remodeling.The biological function and role of YKL-40 is not yet fully understood.It is possible involved in the inflammatory response of asthma,airway hyperresponsiveness,airway remodeling process.The detection of YKL-40 may have some significance in the aided diagnosis,asthma severity and predicting prognosis.

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咳嗽变异性哮喘(cough variant asthma,CVA)是指以慢性咳嗽为主要或唯一症状的一种特殊类型哮喘,其病理生理改变与典型哮喘相同,若未及时诊治,约30%~40%可发展成为典型哮喘。气道炎细胞浸润和气道重塑是 CVA 的病理基础。CVA 可称之为一种隐匿性哮喘,常被临床医师所忽略,患者失去正确的诊断与治疗。正确认识 CVA 的病理生理特征,对临床诊断和治疗具有重要的指导意义,可降低典型哮喘的发病率。本文就 CVA 与气道炎性反应和气道重塑的关系作一综述。
Cough variant asthma(CVA)is a special typologic bronchial asthma (asthma)which presents solely with chronic cough.CVA is a form of asthma,CVA shares a number of pathophysiological features with classic asthma. More importantly,30% to 40% of adult patients with CVA,unless adequately treated,may progress to classic asthma. Cellular infiltration and airway remodeling are pathological basis of CVA.CVA may call an insidious asthma,it was neglected freguently by clinician,and the patients were missed correct diagnosis and treatment.To know correctly pathophysiological features of CVA,it is important significance for clinical treatment,and may decrease incidence of asthma.In this review,we analyzed the correlation between CVA and inflammatory reaction,airway remodeling.

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