外泌体在慢性气道炎症性疾病诊疗中的研究进展

外泌体是一类拥有磷脂双分子层结构的纳米大小的囊形小体, 几乎所有类型细胞都可以分泌。外泌体可通过相关的生物活性物质(DNA、microRNA和蛋白质等)与靶细胞相互作用而实现信息传递和功能调控。以慢性阻塞性肺疾病及支气管哮喘为代表的慢性气道炎症性疾病是常见的呼吸系统疾病, 伴随着对外泌体结构功能持续深入的探究, 人们发现外泌体在气道炎症性疾病进展中发挥着重要作用, 外泌体很可能成为慢性气道炎症性疾病的新型诊断生物标志物、潜在的治疗靶点及药物的载体。本文对外泌体的特性和功能以及在慢性气道炎症性疾病诊疗中的研究进展作一综述。     

慢性阻塞性肺部疾病气道炎症与气道重塑机制的研究

正慢性阻塞性肺部疾病(简称慢阻肺)是一种以持续存在的气流受限为特征,伴气道和肺组织对毒性颗粒或气体的异常炎症反应的常见、多发病。气道重塑是慢阻肺气流阻的重要病理生理机制,目前认为,气道重塑多与气道炎症相伴随。一、气道重塑的病理气道重塑是反复发生的气道损伤和修复导致的气道壁结构改变。它是以气道的平滑肌,上皮细胞,血管和细胞外基质的组织,细胞或分子改变为特征。气道重塑可发生在慢性气道疾病如支气管哮喘,慢     

YKL-40（BRP-39）与支气管哮喘

支气管哮喘（简称哮喘）是-种由多种炎症细胞、炎症因子参与的慢性气道炎症性疾病,Th2分化过度在哮喘气道炎症中起重要作用。YKL40（BRP-39）是新近发现的壳质酶类似物蛋白,参与多种疾病的炎症反应、组织结构重塑等病理过程。YKL-40可通过促进哮喘患者Th2活化、分化并减少其凋亡,增加Th2数量,在哮喘慢性气道炎症中起着重要作用。     

中药对支气管哮喘气道重塑干预机制研究进展

正支气管哮喘(简称哮喘)是最常见的慢性呼吸系统疾病之一,以持续性慢性气道炎症、气道高反应性、气道重塑为主要特点。气道重塑是哮喘的重要特征之一,它是指气道炎症、组织损伤及随后不正常修复导致气道壁结构的改变~([1])。气道重塑的病理改变主要有:气道上皮细胞的改变、炎性细胞浸润、杯状细胞增生、气道平滑肌细胞(ASMC)增殖与迁移、成纤维细胞数量增多、细胞外基质(ECM)沉积、气道     

YKL-40(BRP-39)与支气管哮喘

支气管哮喘(简称哮喘)是一种由多种炎症细胞、炎症因子参与的慢性气道炎症性疾病,Th2分化过度在哮喘气道炎症中起重要作用.YKL-40(BRP-39)是新近发现的壳质酶类似物蛋白,参与多种疾病的炎症反应、组织结构重塑等病理过程.YKL-40可通过促进哮喘患者Th2活化、分化并减少其凋亡,增加Th2数量,在哮喘慢性气道炎症中起着重要作用.     

血栓素A2与慢性肺部炎症性疾病

在慢性阻塞性肺疾病、支气管哮喘和肺囊性纤维化等气道慢性炎症性疾病中,常伴有广泛的气道结构破坏、重塑和黏液高分泌等病理改变.炎症介质血栓素A2(TXA2)是花生四烯酸的环氧合酶代谢产物之一,因其诱导血小板聚集、收缩血管及呼吸道平滑肌和刺激气道及血管平滑肌增殖而在这些病理改变中起着重要作用.TXA2作为一种重要的炎症介质,能刺激血管收缩,进而引起气道微血管渗漏,气道黏液增多,刺激气道平滑肌收缩进而引起气道阻力增加,并参与多种肺部炎症反应,近来还发现其可能参与杯状细胞化生和黏液分泌.现就其在肺部炎性疾病的作用作一综述.     

支气管上皮细胞在支气管哮喘发病中的作用

支气管哮喘(简称哮喘)是一种由多细胞,多细胞组分参与形成的慢性气道炎症性疾病。支气管上皮细胞是气道结构细胞作为抵抗外界损伤因素的第一道防线,当吸入性刺激物质时,首先激化支气管上皮细胞并破坏上皮细胞的正常结构和生理功能,应激状态下的上皮细胞通过分泌炎性介质与自身细胞或其他气道结构细胞、炎性细胞、抗原递呈细胞等相互作用,积极参与哮喘的气道慢性炎症发生与发展进程。     

慢性阻塞性肺疾病气道重塑的研究进展

正慢性阻塞性肺疾病(慢阻肺)简称慢阻肺,是一种具有不完全可逆性性气流受限的肺部疾病,并呈持续性、渐进性加重。慢阻肺作为慢性气道炎症性疾病,有害气体或有害颗粒对气道和肺组织导致的长期慢性炎症及气道重构是其主要的病理特征。目前普遍认为,慢性气道炎症与气道重塑反复发生并不断进展的损伤-修复过程是导致慢阻肺患者持续气流受限的主要原因之一。慢阻肺气道重塑在小气道(内径2mm)更为     

单核细胞迁移募集与肺部感染和炎症

<正>感染是呼吸系统慢性疾病发生及急性加重的常见原因,如慢性阻塞性肺疾病(慢阻肺)和支气管哮喘[1]。目前普遍认为巨噬细胞作为重要的效应细胞之一,在慢阻肺气道炎症启动中起决定性的作用。感染发生后巨噬细胞在气道壁和管腔内大量聚集、激活,释放炎症因子、介导蛋白酶/抗蛋白酶失衡,进而引起组织损伤和肺气肿形成[2][3]。支气管哮喘是树突状细胞(Dendritic cell,DCs)介导的以Ⅱ型辅助性T细胞(Th2)优势免疫为特征的慢性气道变应性疾病     

Toll样受体4与气道慢性炎症性疾病

气道慢性炎症性疾病如慢性阻塞性肺疾病、支气管哮喘等是在各种内外界刺激因素作用下由气道固有细胞、炎症细胞和炎症因子参与的非特异性炎症性疾病.迄今已发现11种Toll样受体(TLR),均为I型跨膜受体蛋白,广泛表达于支气管上皮细胞、支气管平滑肌细胞、树突状细胞、肺泡巨噬细胞等,因其能感知病原体并直接或间接作出防御反应而在慢性气道炎症性疾病的发生发展中发挥重要作用,其中又以TLR4的作用最为突出而成为研究的热点.故深入认识TLR4与慢性气道炎症性疾病的关系将为临床治疗开辟广阔的前景.     

吸烟、肿瘤坏死因子及其受体与慢性阻塞性肺疾病

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)发病率高.发病机制不清.外界环境的刺激导致气道和血管损伤与修复的失平衡可能与COPD的发生相关.其中吸烟致细胞因子、炎症细胞及炎症介质增多,气道和肺实质慢性炎症,导致气道损伤和重构.最终导致气流受限,在肺气肿的形成中起主要作用.肿瘤坏死因子a是重要的炎症因子,通过其主要受体肿瘤坏死因子受体1参与COPD的形成,在COPD的发生、发展中起重要作用.     

Bronchial epithelial cells: The key effector cells in the pathogenesis of chronic obstructive pulmonary disease?

The primary function of the bronchial epithelium is to act as a defensive barrier aiding the maintenance of normal airway function. Bronchial epithelial cells (BEC) form the interface between the external environment and the internal milieu, making it a major target of inhaled insults. However, BEC can also serve as effectors to initiate and orchestrate immune and inflammatory responses by releasing chemokines and cytokines, which recruit and activate inflammatory cells. They also produce excess reactive oxygen species as a result of an oxidant/antioxidant imbalance that contributes to chronic pulmonary inflammation and lung tissue damage. Accumulated mucus from hyperplastic BEC obstructs the lumen of small airways, whereas impaired cell repair, squamous metaplasia and increased extracellular matrix deposition underlying the epithelium is associated with airway remodelling particularly fibrosis and thickening of the airway wall. These alterations in small airway structure lead to airflow limitation, which is critical in the clinical diagnosis of chronic obstructive pulmonary disease (COPD). In this review, we discuss the abnormal function of BEC within a disturbed immune homeostatic environment consisting of ongoing inflammation, oxidative stress and small airway obstruction. We provide an overview of recent insights into the function of the bronchial epithelium in the pathogenesis of COPD and how this may provide novel therapeutic approaches for a number of chronic lung diseases.     

The airway epithelium: more than just a structural barrier

The mammalian airway is lined by a variety of specialized epithelial cells that not only serve as a physical barrier but also respond to environment-induced damage through the release of biologically active factors and constant cellular renewal. The lung epithelium responds to environmental insults such as pathogens, cigarette smoke and pollution by secreting inflammatory mediators and antimicrobial peptides, and by recruiting immune cells to the site of infection or damage. When the epithelium is severely damaged, basal cells and Clara cells that have stem-cell-like properties are capable of self-renewal and proliferation in the affected area, to repair the damage. In order to effectively fight off infections, the epithelium requires the assistance of neutrophils recruited from the peripheral circulation through transendothelial followed by transepithelial migration events. Activated neutrophils migrate across the epithelium through a series of ligand-receptor interactions to the site of injury, where they secrete proteolytic enzymes and oxidative radicals for pathogen destruction. However, chronic activation and recruitment of neutrophils in airway diseases such as chronic obstructive pulmonary disease and asthma has been associated with tissue damage and disease severity. In this paper, we review the current understanding of the airway epithelial response to injury and its interaction with inflammatory cells, in particular the neutrophil.     

炎性因子在慢性阻塞性肺疾病气道炎症中的作用

COPD是一种以气道慢性炎症为特征之一的慢性呼吸系统疾病,气道炎性反应在COPD占有重要作用。炎性细胞因子是机体内最重要的一类细胞因子,多种炎性细胞因子参与气道炎症的病理生理机制,对肺组织和支气管产生损害,并发肺外效应。在COPD的自然病程中存在炎性细胞因子网络系统,调控COPD的气道炎症的发生发展。     

巨噬细胞的极化分型在慢性阻塞性肺疾病中的研究进展

巨噬细胞是单核巨噬细胞系统的终末分化细胞,由单核细胞分化而来。巨噬细胞通过吞噬作用参与非特异性免疫,在适应性免疫中主要发挥免疫调节及抗原递呈功能,从而影响机体全身代谢、造血、血管生成、凋亡、肿瘤和生殖等多种进程。COPD是一种机体对吸烟或吸入其他有害气体、颗粒物引起的异常炎症反应,病理学定义为持续存在的气流受限。它包括一系列病理过程,如大气道的炎症（慢性支气管炎）和小气道的气道重塑、弹性减退和肺间质的破坏造成的肺气肿。尽管引起炎症和肺部组织损伤的原因没有完全研究清楚,但单核巨噬细胞通过释放炎性介质在引起肺部炎症和肺气肿的过程中起到了关键的作用。巨噬细胞因其所处微环境的不同存在不同的分型,而且这种分型在COPD中也有了一定的进展,但吸烟对于巨噬细胞极化分型的影响仍颇有争议。现就巨噬细胞的极化分型在COPD中的研究进展综述如下。     

过氧化物酶体增殖物激活受体γ与肺部疾病的研究进展

过氧化物酶体增殖物激活受体γ（PPARγ）是Ⅱ型核受体超家族成员之一,它在脂肪组织、肺上皮细胞、黏膜下层和气道平滑叽巾都有表达。PPARγ具有多种生物学效应,促进脂肪细胞分化和脂肪生成。增强机体对胰岛素的敏感性,调节体内糖平衡;抑制炎症因子生成及炎症形成;抑制肿瘤生长及纤维化形成等。PPARγ在支气管哮喘、慢性阻塞性肺疾病及肺纤维化等呼吸系统疾病发生、发展中都起到一定的作用。     

Blood platelets and inflammation: their relationship with liver and digestive diseases

An expansion of knowledge from basic and clinical research has highlighted the critical role of platelets in inflammation and tissue repair in addition to their established contribution to hemostasis. Activated platelets are a rich source of mediators participating to inflammation and tissue regeneration. Platelet-derived microparticles recapitulate essential platelet functions and their contribution to the pathogenesis of inflammatory diseases has been emphasized. Recent findings suggest that platelets are both friends and foes for the liver. Platelets are essential to liver regeneration, platelet-derived serotonin being critical. However platelets can also exacerbate liver damage, as in immune-mediated injury. The dual role of platelets has recently been exemplified in animal models of liver fibrosis. Platelets release profibrogenic mediators, such as CXC Chemokine Ligand 4, that is instrumental in the progression of liver fibrosis. On the other hand, thrombocytopenia aggravates liver fibrosis, an outcome linked to the downregulation of hepatic stellate cell collagen production by platelet derived hepatocyte growth factor. CD154, a key molecule in inflammation, is expressed by platelets and is a pathogenic mediator in inflammatory bowel disease. Here, we summarize some of the mechanisms linking platelets with inflammation and comment few recent articles indicating why platelets may prove to be important pathogenic mediators in liver and gastrointestinal diseases.