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福氏志贺菌是发展中国家引起痢疾的主要致病菌。福氏志贺菌O-抗原除噬菌体介导的糖基化和(或)乙酰化外,最近发现一种新的修饰方式磷酸乙醇胺修饰,其机制为由质粒携带的opt基因编码磷酸乙醇胺转移酶在O-抗原的鼠李糖II或(和)鼠李糖III上添加磷酸乙醇胺基团,从而形成血清型Xv、4av和Yv福氏志贺菌,并表达MASF IV-1抗原。人工转化携带opt基因的质粒到无MASF IV-1抗原表达的不同血清型福氏志贺菌中,转化菌株都能表达MASF IV-1抗原。在某些血清型福氏志贺菌中,O-抗原的磷酸乙醇胺修饰与糖基化、乙酰化修饰之间相互作用。现对福氏志贺菌的O-抗原磷酸乙醇胺修饰机制及其与糖基化、乙酰化修饰间的相互作用进行了综述。
Shigella flexneri is the leading cause of dysentery in developing countries. In addition to phage-mediated glycosylation and / or acetylation of Shigella flexneri O-antigen, a new modification of phosphofructokinase was recently discovered by a mechanism by which the opt gene carried by the plasmid encodes phosphoethanolamine transferase Phosphatidylethanolamine groups were added to the r-Saccharide II or (and) rhamnose III of the O-antigen to form serotypes Xv, 4av and Yv. Shigella flexneri and to express the MASF IV-1 antigen. The plasmids carrying the opt gene were artificially transformed into different serotypes of Shigella flexneri in which no MASF IV-1 antigen was expressed, and the transformed strain was capable of expressing the MASF IV-1 antigen. In some serotypes of Shigella flexneri, the phosphoethanolamine modification of the O-antigen interacts with glycosylation, acetylation modifications. The mechanism of O-antigen Phosphoethanolamine modification of Shigella flexneri and its interaction with glycosylation and acetylation modification are reviewed.