胸膜肺炎放线杆菌RTX毒素ApxI的N端结构域在小鼠中引发保护性免疫。
The N-terminal domain of RTX toxin ApxI of Actinobacillus pleuropneumoniae elicits protective immunity in mice.
作者信息
Seah J N, Frey J, Kwang J
机构信息
Laboratory of Animal Health Biotechnology, Temasek Life Sciences Laboratory, The National University of Singapore, Singapore 117604, Singapore.
出版信息
Infect Immun. 2002 Nov;70(11):6464-7. doi: 10.1128/IAI.70.11.6464-6467.2002.
Abstract
We expressed three Actinobacillus pleuropneumoniae ApxI deletion derivatives to map the domain that could induce protective immunity. Antiserum to ApxI N-terminal covered by residues 40 to 380 was found to neutralize ApxI hemolytic activity but not ApxIII cytotoxicity. When used as a subunit vaccine in mice, this recombinant N-terminal fragment elicited protection against lethal infection with heterologous A. pleuropneumoniae serovars.
摘要
我们表达了三种胸膜肺炎放线杆菌ApxI缺失衍生物，以确定可诱导保护性免疫的结构域。发现针对由40至380位残基覆盖的ApxI N末端的抗血清可中和ApxI溶血活性，但不能中和ApxIII细胞毒性。当用作小鼠亚单位疫苗时，这种重组N末端片段可诱导针对异源胸膜肺炎放线杆菌血清型致死感染的保护作用。
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