Community-Acquired Respiratory Distress Syndrome Toxin: Unique Exotoxin for M. pneumoniae.
Community-Acquired Respiratory Distress Syndrome Toxin: Unique Exotoxin for M. pneumoniae.
复制标题
DOI：
10.3389/fmicb.2021.766591
复制
发表时间：
2021
影响因子：
5.2
通讯作者：
He J
中科院分区：
文献类型：
--
作者：
Su X;You X;Luo H;Liang K;Chen L;Tian W;Ye Z;He J
肺炎支原体感染经常导致人类呼吸道疾病，特别是患有非典型肺炎和社区获得性肺炎(CAP)的儿童和成人，并经常与其他肺部疾病，如哮喘、支气管炎和慢性阻塞性肺疾病合并感染而加剧。社区获得性呼吸窘迫综合征毒素(CADS TX)是肺炎支原体唯一产生的外毒素，其ADP核糖基转移酶(ADPRT)活性和细胞空泡化特性已被广泛研究。此外，CARDS TX可诱导炎症反应，导致细胞肿胀、核溶解、粘液增殖和细胞空泡化。卡片TX通过与宿主受体结合进入宿主细胞，然后反向运输到内质网，发挥其致病作用。本文就其结构特点、功能活性、分布和受体、细胞进入机制以及炎症反应等方面进行了综述。总之，本综述的结果为进一步研究肺炎支原体的感染机制以及临床诊断和疫苗的发展提供了理论基础。
Mycoplasma pneumoniae infection often causes respiratory diseases in humans, particularly in children and adults with atypical pneumonia and community-acquired pneumonia (CAP), and is often exacerbated by co-infection with other lung diseases, such as asthma, bronchitis, and chronic obstructive pulmonary disorder. Community-acquired respiratory distress syndrome toxin (CARDS TX) is the only exotoxin produced by M. pneumoniae and has been extensively studied for its ADP-ribosyltransferase (ADPRT) activity and cellular vacuolization properties. Additionally, CARDS TX induces inflammatory responses, resulting in cell swelling, nuclear lysis, mucus proliferation, and cell vacuolization. CARDS TX enters host cells by binding to the host receptor and is then reverse transported to the endoplasmic reticulum to exert its pathogenic effects. In this review, we focus on the structural characteristics, functional activity, distribution and receptors, mechanism of cell entry, and inflammatory response of CARDS TX was examined. Overall, the findings of this review provide a theoretical basis for further investigation of the mechanism of M. pneumoniae infection and the development of clinical diagnosis and vaccines.
登录
查看更多内容
影响因子：
6.4
作者：
Bose S;Segovia JA;Somarajan SR;Chang TH;Kannan TR;Baseman JB
通讯作者：
Baseman JB
ADP-核糖基转移酶和 ADP-核糖基化系统的自然历史。
影响因子：
--
作者：
Aravind L;Zhang D;de Souza RF;Anand S;Iyer LM
通讯作者：
Iyer LM
通过ADP-核糖基毒素，精氨酸特异性的单ADP-核糖基化抗菌肽的体外。
影响因子：
3.7
作者：
Castagnini M;Picchianti M;Talluri E;Biagini M;Del Vecchio M;Di Procolo P;Norais N;Nardi-Dei V;Balducci E
通讯作者：
Balducci E
影响因子：
3.4
作者：
Balasubramanian, Sowmya;Pandranki, Lavanya;Kannan, Thirumalai R.
通讯作者：
Kannan, Thirumalai R.
影响因子：
2.8
作者：
Feng, Monica;Schaff, Andrew C.;Balish, Mitchell F.
通讯作者：
Balish, Mitchell F.