Clinical Core

肺炎支原体在急性和慢性哮喘中的作用仍然难以捉摸；然而，多个品系 有证据表明支原体与慢性哮喘、哮喘加重和长期减退有关。 肺功能提示这种微生物可能在哮喘中起重要作用。本病的诊断。 然而，肺炎支原体感染是困难的，因为肺炎支原体是一种挑剔的有机体，能够 细胞外和细胞内的寄生/持久性，因此，微生物生长直接来自临床 样本几乎总是失败的。活动性肺炎支原体的诊断在以下情况下变得更加困难 在慢性运输中，生物体的负担会显著降低。最近，我们的小组发现了一种M。 肺炎ADP-核糖化/空泡毒素称为社区获得性呼吸窘迫 综合征毒素(CADS TX)，并建立了特异扩增CADS基因的PCR探针(MPN372) 序列。在最近爆发的支原体社区获得性肺炎中，疾病中心 控制和预防表明，对卡片TX的聚合酶链式反应是最敏感的检测方法。一位少校 了解肺炎支原体在哮喘中的作用一直是相对缺乏敏感性的 方法检测肺炎支原体，但不了解肺炎支原体的免疫调节作用。 肺炎感染。使用敏感的聚合酶链式反应和抗原捕获试验来检测卡介苗TX，我们已经 能够证明43.6%的哮喘急性加重成人受试者MPN372呈阳性 实时定量聚合酶链式反应与11%的非喘息性肺病患者和4%的正常健康人的对比 对照组(P&lt；.001急性哮喘与对照组)。此外，我们还建立了一个临床研究网站，以 对顽固性哮喘患者进行了跟踪调查，发现30/62名受试者(48%)的卡介苗Tx呈聚合酶链式反应阳性， 10%的人在10.3个月的平均时间内保持积极。其中三分之二的人一直是积极的 受试者从未出现过对支原体的免疫球蛋白反应(对TX或PI粘附素卡)。这个 临床核心将进行一项纵向研究，以收集TX+/-哮喘患者以及 卡片TX+/-健康对照确定肺炎支原体在哮喘严重性和控制中的作用以及 哮喘患者与健康人群对肺炎支原体免疫应答的差异 非哮喘对照组。

The role of Mycoplasma pneumoniae in acute and chronic asthma remains elusive; however, multiple lines of evidence linking Mycoplasma to chronic asthma, exacerbations of asthma, and long-term decrements In pulmonary function suggest this organism may play an important role in asthma. The diagnosis of M. pneumoniae infection, however, is difficult because M. pneumoniae is a fastidious organism, capable of extracellular and intracellular parasitism/persistence, and therefore, microbiological growth directly from clinical specimens almost always fails. The diagnosis of active M. pneumoniae becomes even more difficult in states of chronic carriage where organism burdens would be significantly lower. Recently, our group identified a M. pneumoniae ADP-ribosylating/vacuolating toxin known as the Community Acquired Respiratory Distress Syndrome Toxin (CARDS TX) and created a PCR probe (MPN372) specific for amplifying cards gene sequences. In a recent outbreak of Mycoplasma community-acquired pneumonia, the Centers for Disease Control and Prevention demonstrated that PCR to CARDS TX was the most sensitive assay tested. A major barrier for understanding the role of M. pneumoniae in asthma has been the relative absence of a sensitive method to detect M. pneumoniae and a failure to understand the specific immunomodulatory role of M. pneumoniae infection. Using sensitive PCR and antigen capture assays to detect CARDS TX, we have been able to demonstrate that 43.6% of adult subjects with acute exacerbations of asthma are positive to MPN372 by real-time PCR versus 11% of subjects admitted with non-asthmatic lung disease and 4% in normal healthy controls (p<.001 for acute asthma vs controls). Additionally, we have established a clinical research site to follow subjects with refractory asthma and found 30/62 subjects (48%) were PCR positive for CARDS TX, with 10% remaining persistently positive over a mean period of 10.3 months. Two thirds of these persistently positive subjects never mounted an IgG response to Mycoplasma (ELISA to either CARDS TX or PI adhesin). The Clinical Core will undertake a longitudinal study to collect samples on both CARDS TX +/- asthmatics as well as CARDS TX +/- healthy controls to establish the role of M. pneumoniae in asthma severity and control as well as the differences in the immunologic responses to M. pneumoniae in asthmatic subjects compared to healthy non-asthmatic controls.