Mycoplasma pneumoniae Infection in Patients with Chronic Asthma

哮喘是一种复杂的疾病，因为它涉及遗传易感性、环境因素和 在疾病的发展和进展中与免疫状态的相互作用。超过1500万 美国人患有这种疾病，尽管使用了强效药物，但仍有16%-17%的人 患者每天都会出现持续且频繁的夜间症状。一个被低估了的人 哮喘病因学中有争议的因素是非典型细菌感染的作用，如那些 肺炎支原体引起的，在启动、加重和延长呼吸道相关中起作用 症状和病理。多条证据直接将肺炎支原体与肺炎的发病机制联系起来 哮喘不能作为哮喘急性加重的诱发因素。儿童肺炎支原体 感染被证明在慢性肺损伤消退后会持续很长一段时间 呼吸道症状。研究表明，高达50%的患者肺功能测试异常 肺炎支原体发作几个月至几年后37%的儿童和肺部异常 呼吸道感染。众所周知，肺炎支原体还可以诱导许多炎症介质。 与哮喘的发病机制有关。免疫球蛋白、白介素4和白介素5已被证明在 肺炎支原体感染儿童，提示肺炎支原体可诱导TH-2样细胞因子 回应。在成人中，在很大比例的稳定型肺炎患者中发现了肺炎支原体 中度重度慢性哮喘。这一发现的意义得到了一项随机、双盲研究的支持 研究表明，只有PCR阳性的哮喘患者在以下情况下改善了他们的肺功能测试 使用针对支原体的抗生素治疗。 最近，巴斯曼博士和卡南博士发现了肺炎支原体的一种adp-核糖化空泡化毒素。 指定为社区获得性呼吸窘迫综合征毒素(卡片TX)。卡TX 在急性和慢性胰腺炎患者中，似乎比P1粘附素分子具有更强的免疫原性 慢性哮喘和卡片fx基因聚合酶链式反应分析似乎也是一个明显的改善现有的M。 肺炎支原体聚合酶链式反应检测患者标本中肺炎支原体该项目旨在 用聚合酶链式反应检测鼻腔灌洗液中卡介苗TX抗体和检测卡介苗DMA值， 各组急、慢性哮喘患者的痰和血清。具体来说，我们将 评估慢性缓解期哮喘患者、哮喘急性加重患者和一组哮喘患者 患有难治性哮喘。我们计划将CARDS TX的灵敏度与“金”标准P1法进行比较 肺炎支原体，并评估这些哮喘患者的细胞和细胞因子反应。

Asthma is a complex disease since it involves genetic predisposition, environmental factors, and an interaction with the immune status in the development and progression of the disease. Over 15 million Americans are afflicted with this disease and despite the use of potent medications, between 16-17% of patients experience continuous daily and frequent nocturnal symptoms. One underappreciated and controversial factor in the etiology of asthma is the role that atypical bacterial infections, such as those caused by Mycoplasma pneumoniae, play in initiating, exacerbating and prolonging airway-related symptoms and pathologies. Multiple lines of evidence directly link M. pneumoniae to the pathogenesis of asthma beyond its role as a precipitating factor in acute exacerbation of asthma. In children, M. pneumoniae infections have been shown to induce chronic lung damage for prolonged periods after the resolution of respiratory tract symptoms. Studies have demonstrated abnormal pulmonary function tests in up to 50% of children and abnormalities of the lung in 37% of children months to years after an episode of M. pneumoniae respiratory infection. Mycoplasma pneumoniae is also known to induce a number of inflammatory mediators implicated in the pathogenesis of asthma. IgE, IL-4, and IL-5 have been shown to be significantly elevated in children with M. pneumoniae infections, suggesting that M. pneumoniae can induce a TH-2 like cytokine response. In adults, M. pneumoniae has been detected in a large percentage of patients with stable moderately severe chronic asthma. The significance of this finding was supported by a randomized, doubleblind study that demonstrated only PCR positive asthmatics improved their pulmonary function test when treated with antibiotic therapy directed against mycoplasmas. Recently, Drs. Baseman and Kannan discovered an ADP-ribosylating, vacuolating toxin of M. pneumoniae designated the Community Acquired Respiratory Distress Syndrome Toxin (CARDS TX). CARDS TX appears to be much more immunogenic than the P1 adhesin molecule in patients with both acute and chronic asthma, and cards fxgene PCR assays also appear to be a marked improvement over existing M. pneumoniae PCR assays in detecting M. pneumoniae in patient samples. This project is designed to evaluate the prevalence of antibodies to CARDS TX and detect cards tx DMA by PCR in nasal lavage, sputum, and serum in various groups of patients with acute and chronic asthma. Specifically, we will evaluate chronic stable asthmatics, patients with acute exacerbation of asthma, and a group of asthmatics with refractory asthma. We plan to compare the sensitivity of CARDS TX to the "gold" standard P1 assay for M. pneumoniae and to evaluate the cellular and cytokine response in these groups of asthmatic patients.