肺微生物组学在常见肺部疾病中的作用研究进展

肺微生物组学的研究是近年来肺部疾病研究领域的热点,并有多篇研究在国际重要的学术期刊上发表.他们旨在研究肺部微生物的组成、多样性及其与人类健康和疾病的相关性,尤其是与慢性肺部疾病的相关性.本文就肺微生物组学在常见肺部疾病中的作用和最新的研究进展进行了综述,希望能为临床和科研带来帮助.     

从药理药效看支气管舒张药物的选择

阻塞性肺部疾病(包括支气管哮喘和慢性阻塞性肺疾病)的特征是气流受限。支气管舒张药物可通过松弛气道平滑肌(舒张支气管)减轻患者气流受限症状,减少呼吸困难并改善生活质量。本文重点讨论支气管舒张剂在支气管哮喘和慢性阻塞性肺疾病中的药理特性及使用,以进一步增加临床医师对支气管舒张剂特异性和安全性的认知。     

经纤支镜支气管肺泡灌洗术治疗急性呼吸衰竭在重症监护病房的临床应用

目的 探讨经纤维支气管镜支气管肺泡灌洗术治疗急性呼吸衰竭在重症监护病房的临床应用效果.方法 选择胸科术后、颅脑术后、创伤昏迷、慢性阻塞性肺疾病患者共35例,均有明显的气道分泌物排出困难、肺不张、肺部感染伴呼吸衰竭、急性呼吸衰竭的表现,均经常规氧疗、抗感染、解痉、平喘、化痰或机械通气等治疗无效后,在重症监护病房采用床旁纤支镜气管吸引及支气管肺泡灌洗、局部注射药物治疗,并监测心电、血压、呼吸、血氧饱和度变化及进行血气分析.结果 所有病例经治疗后,临床症状改善,血气分析PaO2、SaO2与治疗前相比有明显增高(P<0.05).结论 纤支镜气道吸引、支气管肺泡灌洗、局部注射药物的疗法效果确切,能迅速缓解患者因气道阻塞所致肺不张、呼吸困难,有利于气道管理和肺部感染的控制,明显缩短了患者留住重症监护病房的时间及住院周期,降低了住院费用,值得临床推广.     

白介素13与气道高反应性

气道高反应性是呼吸道疾病最常见的临床表现，它是气道对非特异性刺激反应亢进的一种状态，与气道炎症、气道重构相并列，是支气管哮喘的重要病理变化之一。而在肺部的其它疾病，如慢性阻塞性肺疾病、急性支气管炎、支气管扩张、过敏性肺炎、肺结核等也有不同程度的表现。目前认为气道炎症是气道高反应性的重要基础，尤其是Th2型细胞因子IL-4、IL-13、IL-5、IL-9、IL-10等的增多，     

真菌与临床喘息性疾病

真菌与喘息性疾病的发病有密切关系.自然界空气中真菌孢子可诱发支气管哮喘急性加重.真菌在下呼吸道定植或感染同样可导致气道致敏从而诱发喘息.真菌还可增加气道内痰液量及黏稠度,导致小气道不完全栓塞.临床上与真菌密切相关的喘息性疾病包括支气管哮喘、过敏性支气管肺曲霉病(过敏性支气管肺真菌病)、慢性阻塞性肺疾病以及支气管扩张等结构性肺病.治疗真菌相关喘息首选糖皮质激素,但在急性发作期尚无吸入激素有效的证据.大部分患者可从抗真菌治疗中得益.     

真菌与临床喘息性疾病

真菌与喘息性疾病的发病有密切关系.自然界空气中真菌孢子可诱发支气管哮喘急性加重.真菌在下呼吸道定植或感染同样可导致气道致敏从而诱发喘息.真菌还可增加气道内痰液量及黏稠度,导致小气道不完全栓塞.临床上与真菌密切相关的喘息性疾病包括支气管哮喘、过敏性支气管肺曲霉病(过敏性支气管肺真菌病)、慢性阻塞性肺疾病以及支气管扩张等结构性肺病.治疗真菌相关喘息首选糖皮质激素,但在急性发作期尚无吸入激素有效的证据.大部分患者可从抗真菌治疗中得益.     

氧化应激与支气管哮喘气道黏液高分泌研究进展

哮喘是一种以支气管收缩可逆性、肺部炎症及气道重塑为特点的慢性气道炎症性疾病.黏液过度分泌导致气道阻塞、肺功能下降、气道重塑和感染增加.过度的活性氧/活性氮(ROS/RNS)产生造成气道炎症,气道高反应性,气道微血管高通透性和气道黏液高分泌,以及组织损伤和形态的改变.减轻氧化应激或增加抗氧化能够减轻气道嗜酸粒细胞,减少黏液分泌,减轻支气管高反应性.本文就氧化应激与哮喘气道黏液高分泌的关系作一综述.     

氧化应激与支气管哮喘气道黏液高分泌研究进展

哮喘是一种以支气管收缩可逆性、肺部炎症及气道重塑为特点的慢性气道炎症性疾病.黏液过度分泌导致气道阻塞、肺功能下降、气道重塑和感染增加.过度的活性氧/活性氮(ROS/RNS)产生造成气道炎症,气道高反应性,气道微血管高通透性和气道黏液高分泌,以及组织损伤和形态的改变.减轻氧化应激或增加抗氧化能够减轻气道嗜酸粒细胞,减少黏液分泌,减轻支气管高反应性.本文就氧化应激与哮喘气道黏液高分泌的关系作一综述.     

支气管哮喘与小气道炎症的研究进展

支气管哮喘是常见的慢性呼吸道疾病之一,患病率在全球范围内有逐年增加趋势.1922年Hubert和Koessler第1次描述了重症哮喘存在气道重塑[1].2002年,全球哮喘防治创意(GINA)提出,无论轻重度哮喘,大小气道均存在急性和慢性炎症,各级气道都存在气道重塑.近年来,哮喘的小气道炎症研究受到学术界的广泛重视,国内外在哮喘与小气道炎症方面进行了大量研究.我们就哮喘小气道炎症进展作一综述.     

低剂量CT空气潴留指标用于支气管哮喘患者病情分析

支气管哮喘(bronchial asthma)是一种常见的以气道慢性炎症为主要特征的慢性气道疾病,常在夜间及凌晨发作或加重,中重度支气管哮喘可严重影响患者生活质量,威胁患者生命安全[1] .在支气管哮喘的治疗过程中根据不同哮喘分级予以不同治疗方案以达到良好控制症状、改善气流受限及降低患者支气管哮喘加重的风险[2] .准...     

气道微生态在慢性阻塞性肺疾病中的研究进展

慢性阻塞性肺疾病（COPD）是一种慢性气道炎症性疾病,其特征为慢性呼吸道症状（呼吸困难、咳嗽、咳痰、急性加重）。感染是COPD恶化以及肺功能下降的主要原因,呼吸道微生态以及其所带来的免疫调节功能在其中发挥重要作用。新一代基因测序技术使得更清楚地了解呼吸道微生态组成及其与呼吸系统疾病相关性,不仅揭示了健康人群肺部拥有丰富的微生物群落,而且与健康人群相比,COPD患者的气道微生态结构和各菌群的相对丰度均发生了改变。本文对气道微生态在COPD中的研究进展作一综述。     

Severe pulmonary hypertension in histiocytosis X

Diminished exercise capacity in advanced pulmonary histiocytosis X does not appear to be related to ventilatory limitation but may be related to pulmonary vascular dysfunction. Pulmonary hemodynamics and respiratory function were studied in 21 consecutive patients with advanced pulmonary histiocytosis X, and compared with parameters of patients with other severe chronic lung diseases (29 patients with chronic obstructive pulmonary disease and 14 patients with idiopathic pulmonary fibrosis). All patients with pulmonary histiocytosis X displayed severe pulmonary hypertension: mean pulmonary arterial pressure, 59 +/- 4 mm Hg; cardiac index, 2.6 +/- 0.8 L/min/m(2); and total vascular pulmonary resistance, 25 +/- 3 IU/m(2) (p < 0.05, as compared with patients with other chronic lung diseases). Pa(O(2)) was similar in the three groups, whereas FEV(1) was lower in patients with other chronic lung diseases (p < 0.05). In contrast to other chronic lung diseases, the degree of pulmonary hypertension was not related to variables of pulmonary function in pulmonary histiocytosis X. Histopathology was available for 12 patients with pulmonary histiocytosis X and revealed proliferative vasculopathy involving muscular arteries and veins, with prominent venular involvement. Two consecutive lung samples (taken before and after the occurrence of pulmonary hypertension) were available for six patients with pulmonary histiocytosis X, and showed that pulmonary vasculopathy worsened, whereas parenchymal and bronchiolar lesions remained relatively unchanged. These results indicate that pulmonary hypertension in pulmonary histiocytosis X might be related to an intrinsic pulmonary vascular disease, in which the pulmonary circulation is involved independent of small airway and lung parenchyma injury.     

慢性阻塞性肺疾病呼出气冷凝液中的生物标记物及其意义

呼出气冷凝液(exhaled breath condensate,EBC)是一种无创研究气道内衬液成分的方法,也为评估肺部炎症提供可能.目前普遍认为,慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是以气道、肺实质和肺血管的慢性炎症为特征的疾病.通过对COPD患者EBC的收集和检测,可实现对气道炎症的实时、无创、简单、重复的监测.     

慢性阻塞性肺疾病呼出气冷凝液中的生物标记物及其意义

呼出气冷凝液(exhaled breath condensate,EBC)是一种无创研究气道内衬液成分的方法,也为评估肺部炎症提供可能.目前普遍认为,慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是以气道、肺实质和肺血管的慢性炎症为特征的疾病.通过对COPD患者EBC的收集和检测,可实现对气道炎症的实时、无创、简单、重复的监测.     

Treatments of refractory eosinophilic lung diseases with biologics

Biologics targeting the molecules associated with type 2 inflammation have significantly improved the outcomes of patients with severe eosinophilic asthma and chronic rhinosinusitis with nasal polyps (CRSwNP). Chronic eosinophilic airway/lung diseases including chronic eosinophilic pneumonia, allergic bronchopulmonary aspergillosis/mycosis, eosinophilic bronchitis, and eosinophilic granulomatosis with polyangiitis share clinical features with eosinophilic asthma and CRPwNP, which are mostly adult-onset and may develop simultaneously or consecutively. These eosinophilic airway/lung diseases respond well to initial treatment with systemic corticosteroids, but often recur when the corticosteroids are tapered. The management of these “refractory” cases is an unmet need for clinicians. We first reviewed the standard treatments for these chronic eosinophilic airway/lung diseases, followed by the definition and prevalence of refractory diseases and the role of biologics in their management. The available evidence varies from case reports and case series to randomized control trials, depending on the type of disease; however, these studies provide not only a direction for clinical practice, but also insights into the pathophysiology of each disease. Physicians should discuss the efficacy and costs of biologics in patients with refractory eosinophilic airway/lung diseases to minimize not only the current symptoms, but future risks as well.     

Adenosine signaling in asthma and chronic obstructive pulmonary disease

PURPOSE OF REVIEW: The chronic lung diseases, asthma and chronic obstructive pulmonary disease, are pulmonary disorders in which persistent inflammation and alterations in lung structure contribute to a progressive loss of lung function. Although the exact type of inflammation and damage in each disease is distinct, they share the common feature that they are chronic in nature. Despite efforts, little is known about the cellular and molecular mechanisms that drive the chronicity of these two diseases. This review will summarize important findings regarding the role of adenosine, a signaling nucleoside implicated in the pathogenesis of these two disorders. RECENT FINDINGS: Aerosolized adenosine induces bronchoconstriction in patients with asthma and chronic obstructive pulmonary disease primarily through the release of mast cell mediators. In this setting it can not only be used to aid in diagnosis but also to monitor patient responses to steroid therapy. Adenosine levels are elevated in the lungs of asthma patients, indicating greater flux through adenosine receptor signaling pathways. In-vitro studies have shown adenosine to access pathways leading to the genesis of chronic inflammation via the release of proinflammatory cytokines and chemokines. Animal studies demonstrate that merely elevating adenosine levels in the mouse is sufficient to induce a pulmonary phenotype with features of asthma and chronic obstructive pulmonary disease. SUMMARY: Identifying mediators regulating the chronic nature of asthma and chronic obstructive pulmonary disease is critical towards advancements in treatment options. Adenosine has been implicated in promoting the inflammation and airway remodeling seen in chronic lung disease and thus makes an attractive therapeutic target.     

Clinical aspects of exhaled nitric oxide.

There has been intense research into the role nitric oxide (NO) plays in physiological and pathological mechanisms and its clinical significance in respiratory medicine. Elevated levels of exhaled levels of exhaled NO in asthma and other inflammatory lung diseases lead to many studies examining NO as potential markers of airway inflammation, enabling repeated noninvasive and standardized monitoring of airway inflammation. In airway inflammation, NO is not merely a marker but may have anti-inflammatory and pro-inflammatory effects. Significant correlation has been found between exhaled NO and skin test scores in steroid naive asthmatic patients, allowing to discriminate patients with and without airway responsiveness. Exhaled NO is significantly elevated in acute asthma, or steroid-resistant severe asthma, or when the maintenance dose of inhaled steroids is reduced, and quickly reduced down to the levels in patients with stable asthma after steroid treatment. Exhaled NO has been successfully used to monitor anti-inflammatory treatment with inhaled corticosteroids in asthma. Exhaled NO is extremely sensitive and rapid marker of the dose-dependent effect of steroid treatment, or asthma deterioration, which is increased to any changes in lung function, provocative concentration causing a 20% fall in forced expiratory volume, sputum eosinophilia or asthma symptoms. Exhaled NO is not increased in stable chronic obstructive pulmonary disease (COPD), but patients with unstable COPD, or bronchiectasis have high NO levels. Exhaled and nasal NO are diagnostically low in cystic fibrosis and primary pulmonary dyskinesia. Analysis of exhaled air, including nitric oxide, is feasible and could provide a noninvasive method for use in monitoring and management of lung diseases.     

Inhaled corticosteroids and risk of tuberculosis—How bad is the risk?

Inhaled corticosteroids (ICS) have a central role in the management of obstructive airway diseases. Use of ICS in asthma and chronic obstructive pulmonary disease (COPD) is associated with a small but clear increase in incidence of pneumonia and tuberculosis. Since ICS use in obstructive airway diseases has beneficial effects with regard to symptoms, lung function, quality of life and exacerbations, denying the benefit of ICS solely based on this small elevated risk of pneumonias and tuberculosis is not justified. The present article attempts to elucidate mechanisms contributing to the increased risk, assesses the magnitude and risk factors of tuberculosis in patients using ICS and provides practical suggestions for practising clinicians.     

Radiological Approach to Asthma and COPD-The Role of Computed Tomography

Asthma and chronic obstructive pulmonary disease (COPD) are among the most prevalent lung diseases. In both asthma and COPD, airway inflammation leads to airway remodeling. Parenchyma of the lung is also influenced by disease conditions. Airway wall thickening/lumen narrowing and parenchymal destruction occur in COPD. In asthma, airway remodeling contributes to the lung parenchyma. Computed tomography (CT) has been widely used as an imaging tool for lung diseases. With the technical advancement of CT, together with the development of analysis software, it is now possible to analyze the lung parenchymal change and airway remodeling quantitatively using CT. This article reviews the role of CT in assessing the lung structure and functions of patients with asthma and COPD.     

Pathologic similarities and differences between asthma and chronic obstructive pulmonary disease

PURPOSE OF REVIEW: Classically, asthma and chronic obstructive pulmonary disease present distinct clinical, physiologic and pathologic features. However, not infrequently, patients may present with overlapping clinical symptoms and physiological abnormalities: patients with severe asthma may present with fixed airway obstruction and patients with chronic obstructive pulmonary disease may have hyperresponsiveness and eosinophilia. At pathological level, inflammatory and structural similarities also occur and may be related to the phenotypic overlaps. RECENT FINDINGS: In patients with asthma overlaps at inflammatory level exist with chronic obstructive pulmonary disease, such as increased neutrophilia in patients with severe asthma or an association of CD8+ T cells and lung-function decline. In chronic obstructive pulmonary disease, minimizing eosinophilia may be important to reduce exacerbations. Structural alterations occur in both diseases, but involving airway compartments differently. Airway epithelial changes, extracellular matrix deposition and mucus gland hypertrophy occur in both diseases. Asthmatics have thicker reticular basement membrane and more prominent smooth-muscle abnormalities, whereas emphysema is a distinct feature of chronic obstructive pulmonary disease. SUMMARY: Recognizing the differences and similarities at pathological level in both diseases may lead to a better understanding of the overlapping clinical and physiological phenotypes, thereby helping to better plan specific treatment and long-term management.