Clinical Core

肺炎支原体在急性和慢性哮喘中的作用仍然是难以捉摸的;然而， 支原体与慢性哮喘、哮喘恶化和长期哮喘减少有关的证据 肺功能表明这种微生物可能在哮喘中起重要作用。M. 然而，肺炎支原体感染是困难的，因为M.肺炎是一种挑剔的微生物，能够 细胞外和细胞内寄生/持久性，因此，微生物生长直接来自临床 样品几乎总是失败。活动性M.肺炎变得更加困难， 慢性携带，生物体负担将大大降低。最近，我们的小组确定了一个M。 肺炎ADP-核糖基化/空泡化毒素，称为社区获得性呼吸窘迫 Syndrome Toxin（CRT-TX），并创建了特异性扩增cards基因的PCR探针（MPN372 序列的在最近一次支原体社区获得性肺炎的爆发中， 控制和预防表明，PCR检测CRT-TX是最敏感的检测方法。一个主要 理解M.肺炎在哮喘中一直是相对缺乏一种敏感的 方法检测M.肺炎支原体和未能了解特定的免疫调节作用。 肺炎感染。我们已经使用灵敏的PCR和抗原捕获检测来检测CARDS TX， 能够证明43.6%的哮喘急性加重成人受试者对MPN372呈阳性， 与11%的非哮喘性肺病住院受试者和4%的正常健康受试者相比， 对照组（急性哮喘与对照组相比p <0.001）。此外，我们还建立了一个临床研究中心， 随访难治性哮喘受试者，发现30/62例受试者（48%）为PCR阳性， 10%在平均10.3个月内保持持续阳性。其中三分之二的持续阳性 受试者从未对支原体产生IgG应答（ELISA法检测支原体TX或PI粘附素）。的 临床中心将进行一项纵向研究，以收集哮喘患者的样本， BTX +/-健康对照以确立M.肺炎在哮喘严重程度和控制以及 对M.哮喘受试者与健康受试者相比 非哮喘对照。

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.