Objective To determine the airway wall thickness at the segmental and subsegmental levels in patients with bronchial asthma and eosinophilic bronchitis ( EB) by high resolution CT scanning,and evaluate its relationship with airway hyperresponsiveness. Methods High resolution CT scanning was performed in 14 subjects with asthma,15 subjects with EB, 15 subjects with cough variant asthma ( CVA) ,and 14 healthy volunteers. Total airway and lumen diameter, total airway cross sectional area and lumen area which corrected by body surface area ( BSA) were measured. The percentage of airway wall area to total airway cross sectional area ( WA% ) and wall thickness to airway diameter ratio ( T/D) were calculated for the right upper lobe apical segmental bronchus ( RB1) and all airways clearly visualized with a transverse diameter of 1-6 mm. Results T/D/BSA and WA% in the asthma patients were all significantly higher than those in the subjects with EB, CVA and healthy volunteers. T/D/BSA and WA% in the EB patients were significantly higher than the healthy volunteers, and similar with the CVA patients. Al /BSA in the patientswith asthma and CVA was less than the subjects with EB and the healthy volunteers. However, Al /BSA in the EB patients was similar with the healthy volunteers. Conclusions The airway wall thickness and remodeling can be measured and assessed by high resolution CT. Airway wall thickness and remodeling inEB patients are milder than asthma patients, which may be associated with airway hyperresponsiveness that presents in asthma but not in EB.
Objective To investigate the effects of diesel exhaust particles ( DEP) on the production of CCL11, CCL24 and CCL26 in asthmatic rats. Methods Fifty SD rats were randomly divided into five groups. Group A was an normal control group. The rats in group B, C, D, and E were sensitized and challenged by ovalbumin ( OVA) to establish asthma model. Then the rats in the group C, D, E were inhaled DEP for 1, 2, 3 weeks, respectively. Lung tissue and brouchoalveolar lavage fluid ( BALF) were collected for detection of CCL11, CCL24, and CCL26 expression by ELISA and q-RT-PCR. Results The transcription of CCL 24, CCL26 gene and the production of CCL24 and CCL26 protein increased significantly compared with the control group ( P lt;0. 05) , and were positively associated with the DEP inhalation time. However, CCL11 gene and protein expression were not changed significantly compared with the control. Conclusion The exposure to DEP can induce the production of CCL24 and CCL26 in the asthmaic rats, which might aggravateairway hyperresponsiveness.
嗜酸粒细胞性支气管炎(EB)是一种独立的疾病吗?答案是否定的，现有的证据也不支持。 广义的EB是指气管和支气管壁存在明显嗜酸粒细胞浸润的一种病理状态，为描记气道炎症特征的术语。作为一种常见的发病机制，EB参与多种呼吸系统疾病的发生。哮喘的基本特点就是EB，并与气道高反应性、气道重塑和可逆性气道阻塞密切相关 。除此之外，非哮喘性EB(nonasth— matic eosinophilic bronchitis)、COPD、上气道咳嗽综合征和胃食管反流性咳嗽等均可见EB改变，甚至无下呼吸道症状的变应性鼻炎或部分健康人也存在这种类型的气道炎症。因此，EB在临床上至少存在哮喘、非哮喘性EB、合并COPD 和无症状等表现形式。广义的EB并不是一种疾病，而是多种呼吸道疾病的共同病理过程。 狭义的EB即非哮喘I生EB，是指以咳嗽为唯一症状、肺通气功能和气道反应性正常、诱导痰中嗜酸粒细胞明显增多而皮质激素治疗有效者，是慢性咳嗽的常见病因。目前有观点认为，和咳嗽变异型哮喘相似，EB可能是极轻微的哮喘或哮喘的前期表现。研究发现，EB的病因和发病机制与哮喘很相似。如引起哮喘的环境职业因素和吸入过敏原均可导致EB，Th2炎症反应是两者嗜酸粒细胞气道炎症的主要基础。大部分研究显示介导EB和哮喘的嗜酸粒细胞气道炎症的细胞和细胞因子相同，或仅有程度上的差别。EB和哮喘一样也存在呼出气一氧化氮浓度增加，气道上皮基底膜增厚和上皮下纤维化，气道炎症及气道重塑改变程度两者也相似 。最大的不同在于肥大细胞在气道壁不同部位的浸润和激活。哮喘患者肥大细胞主要浸润支气管平滑肌层，而在EB则主要位于支气管黏膜层 。肥大细胞在气道壁的不同空间分布可以解释哮喘的气道高反应性和EB的咳嗽高敏感性，但不足于据此认为两者为不同的疾病。
Gibson等首先发现7例慢性咳嗽患者表现为慢性刺激性干咳或咳少许黏痰，诱导痰嗜酸粒细胞增高，糖皮质激素治疗效果良好；但患者肺通气功能正常，无气道高反应性 (AHR)，峰流速(PEF)变异率正常，无法诊断为支气管哮喘，因而称之为嗜酸粒细胞性支气管炎(EB)。研究结果发表于 1989年国际著名杂志柳叶刀(Lancet)。从Gibson等提出 EB的诊断以来，受到国内外广大专家的重视，虽然目前对 EB是否是一种独立的疾病或哮喘的早期阶段尚存在一些争议，但愈来愈多的证据表明EB是一种独立的疾病 。下面从EB的定义、病因、病理免疫特征、临床表现、治疗反应及预后等方面对此问题进行讨论，说明EB是一种独立的疾病。
ObjectiveTo explore the effect of Aspergillus fumigatus on airway eosinophilia and hyperresponsiveness in rat model of chronic asthma. MethodsWistar rats were sensitized by intraperitoneal injections with ovalbumin (OVA) followed by chronic inhalation of nebulized OVA or physiologic saline. Rats were administered via the airways with placebo or aerosolized Aspergillus fumigatus spores suspension mimicking chronic Aspergillus fumigatus exposure. The Penh after acetylcholine provocation was detected using WBP system. The concentrations of IL-5 and eotaxin in BALF were measured by ELISA. The extents of eosinophil infiltration were evaluated on hematoxylin and eosin-stained(HE) and Wright-Giemsa stained BALF cells smear. ResultsAspergillus fumigatus worsened allergic airway inflammation in OVA-challenged rats,as evidenced by enhanced bronchial responsiveness to inhaled acetylcholine and increased bronchial eosinophilia. Elevated airway eosinophilia corresponded with higher levels of IL-5 and eotaxin in the Aspergillus Fumigatus exposure group. Aspergillus fumigatus,however,did not affect bronchial responses,numbers of eosinophils,IL-5 and eotaxin levels in saline challenged mice. ConclusionThe Results show that chronic Aspergillus fumigatus exposure aggravates eosinophilic airway inflammation in asthma rats by enhancing IL-5 and eotaxin production. Aspergillus fumigatus also increases bronchial hyperresponsiveness in asthma rats.
ObjectiveTo explore the effects of Aspergillus fumigatus (A. fumigatus) on airway inflammation, airway responsiveness and total serum IgE in asthmatic rats. MethodsEighteen male Wistar rats were divided into three groups randomly, ie. a normal control group, an asthmatic model group, and an A. fumigatus group. The rats in the model group and the A.fumigatus group were sensititized and challenged with ovalbumin to establish asthmatic model. After establishment of asthmatic model, the rats in the A. fumigatus group were treated with chronic A. fumigatus spores inhalation. Subsequently, airway responsiveness/sensitivity to methacholine(Ach), levels of serum IgE and airway inflammation were assessed and compared among three groups. ResultsCompared with the asthmatic rats, the rats treated with A. fumigatus showed higher airway responsiveness (Penh/baselin value was significantly increased at the Mch concentration of 12.5, 25 and 50 mg/mL), increased inflammatory cells infiltration in pulmonary tissue slices and increased serum IgE level (P < 0.05). Most importantly, serum IgE level was detected in close relationship with PC100 which was defined as the dose of Mch causing 100% increase of enhance pause (Penh) value without Mch challenge (r=-0.873, P < 0.01). Serum IgE level was also closely related to the percentage of eosinophils in bronchoalveolar lavage fluid (r=0.937, P < 0.01). ConclusionsChronic A. fumigatus inhalation aggravates airway inflammation, bronchial hyperresponsiveness and serum IgE level in asthma. IgE may play an important role in facilitating the development of bronchial responsiveness and eosinophilic inflammation.
ObjectiveTo explore the cytologic profile of induced sputum and its relationship with the treatment response in patients with chronic obstructive pulmonary disease (COPD). MethodsSixty-five treatment-naive patients with COPD and 26 normal subjects were recruited for the study. Sputums induced by the inhalation of hypertonic saline were collected, and the associations of differential cell counting were analyzed with pulmonary function, modified Medical Research Council dyspnea scale, St. George's Respiratory Questionnaire score (SGRQ) before and after the treatment with inhaled corticosteroid and long-acting β2-agonist. ResultsThe cell percentages of neutrophil (Neu), macrophage, eosinophil (Eos) and lymphocyte in induced sputum of the COPD patients were (86.24±15.04)%, (5.75±6.96)%, (4.71±4.79)%, and (1.30±1.09)%, respectively. The eosinophil percentage (Eos%) was≥3% in 31 patients (60.78%). The neutrophil percentage (Neu%) was inversely correlated with forced expiratory volume in 1 second (FEV1), percent of predicted value of FEV1 (FEV1% pred), forced vital capacity (FVC), and percent of predicted value of FVC (FVC% pred) (P < 0.01, respectively), and positively correlated with the SGRQ symptom score (r=0.304, P=0.034). The Eos% was inversely correlated with FEV1/FVC ratio (r=-0.399, P=0.004). The patients with Eos%≥3% improved significantly in FEV1 and symptom score (P < 0.05, respectively) than the patients with Eos% < 3%. ConclusionsAn eosinophilic airway inflammation is present in a subgroup of COPD. The Eos% is inversely correlated with pulmonary function and may be a predictive indicator of response to treatment with inhaled corticosteroids and long-acting β2-agonists.