肺炎支原体主要黏附蛋白的研究进展

肺炎支原体(Mycoplasma pneumoniae,Mp)可引起呼吸道感染,是儿童社区获得性肺炎的常见致病菌,并且可导致多系统并发症。Mp尖端的黏附蛋白复合体与肺纤毛上皮细胞的黏附过程是其主要致病机制。P1、P30、P116等蛋白作为黏附复合体的主要成分,在感染过程中起到了关键作用。在缺失这些蛋白的突变株中,细胞结构异常,黏附能力、运动速度、致病性均表现出不同程度的下降。由于Mp生长缓慢,对营养要求苛刻,常规微生物分离培养不适用于临床快速诊断,目前亚洲地区Mp耐药率居高不下,Mp感染后又无特异性临床症状,使得临床工作中Mp感染的诊治常被延误。重组蛋白表达技术的出现,使得Mp主要蛋白可以应用在Mp诊断试剂盒和疫苗研发中,本文针对Mp主要黏附蛋白的基因结构、致病机制及其应用方面的最新研究进展进行综述。

Research Progress of the Major Adhesin Proteins of Mycoplasma Pneumoniae

Mycoplasma Pneumoniae,M. Pneumoniae is an important human pathogen that causes primary atypical pneumonia, tracheobronchitis, pharyngitis, asthma and autoimmune diseases. Cytadherence of M. Pneumoniae to respiratory epithelium is essential to tissue colonization and subsequent pathogenesis. It is a complex multifactorial process requiring the specialized tip organelle that possesses a group of adhesin proteins such as P1, P30, P116 and HMW1-3, et al. The adhesin proteins deficient mutants show lower gliding velocity, reduced cytadherence, and decreased steady-state levels of tip organelle. The standard methods for the diagnosis of M. Pneumoniae are culture, serological tests, and PCR. As a fastidious organism, M. Pneumoniae can be difficult to isolate. Considerable cross-reactivity exists between the whole cell antigens used in the commercial serological testing assays. Identification of specific protein antigens is crucial to eliminate the risk of cross-reactions among different related organisms. The adhesin proteins P1 and P30 are also testified to be strongly immunogenic in humans and experimental animals infected with M. Pneumoniae. Expression of adhesin proteins in heterologous expression systems provides an opportunity to explore the roles of these proteins in pathogenicity and contributes to develop diagnostic reagents and vaccines. In this review we discuss the applications of various adhesin proteins of M. Pneumoniae.