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对来自牛源金黄色葡萄球菌的一个假定致病岛的特征分析,该致病岛编码多种超抗原。

Characterization of a putative pathogenicity island from bovine Staphylococcus aureus encoding multiple superantigens.

作者信息

Fitzgerald J R, Monday S R, Foster T J, Bohach G A, Hartigan P J, Meaney W J, Smyth C J

机构信息

Department of Microbiology, Moyne Institute of Preventive Medicine, Republic of Ireland.

出版信息

J Bacteriol. 2001 Jan;183(1):63-70. doi: 10.1128/JB.183.1.63-70.2001.

Abstract

Previous studies have demonstrated that a proportion of Staphylococcus aureus isolates from bovine mastitis coproduce toxic shock syndrome toxin (TSST) and staphylococcal enterotoxin C (SEC). In this study, molecular genetic analysis of one such strain, RF122, revealed the presence of a 15,891-bp putative pathogenicity island (SaPIbov) encoding the genes for TSST (tst), the SEC bovine variant (sec-bovine), and a gene (sel) which encodes an enterotoxin-like protein. The island contains 21 open reading frames specifying hypothetical proteins longer than 60 amino acids including an integrase-like gene. The element is bordered by 74-bp direct repeats at the left and right junctions, and the integration site lies adjacent to the 3' end of the GMP synthase gene (gmps) in the S. aureus chromosome. SaPIbov contains a central region of sequence identity with the previously characterized tst pathogenicity island SaPI1 (J. A. Lindsay et al., Mol. Microbiol. 29:527-543, 1998). A closely related strain, RF120, of the same multilocus enzyme electrophoretic type, random amplified polymorphic DNA type, and ribotype, does not contain the island, implying that the element is mobile and that a recent insertion/deletion event has taken place. TSST and TSST/SEC-deficient mutants of S. aureus strain RF122 were constructed by allele replacement. In vitro bovine Vbeta-specific lymphocyte expansion analysis by culture supernatants of wild-type strains and of tst and sec-bovine allele replacement mutants revealed that TSST stimulates BTB13-specific T cells whereas SEC-bovine stimulates BTB93-specific T cells. This suggests that the presence of SaPIbov may contribute to modulation of the bovine immune response.

摘要

以往研究表明,从牛乳腺炎分离出的一部分金黄色葡萄球菌菌株可共同产生中毒性休克综合征毒素(TSST)和葡萄球菌肠毒素C(SEC)。在本研究中,对一株这样的菌株RF122进行分子遗传学分析,发现存在一个15,891 bp的假定致病岛(SaPIbov),其编码TSST(tst)、SEC牛变体(sec-bovine)的基因,以及一个编码类肠毒素蛋白的基因(sel)。该岛包含21个开放阅读框,指定了长度超过60个氨基酸的假定蛋白包括一个类整合酶基因。该元件在左右连接处由74 bp的直接重复序列界定,整合位点位于金黄色葡萄球菌染色体中GMP合酶基因(gmps)的3'端附近。SaPIbov包含一个与先前鉴定的tst致病岛SaPI1具有序列同一性的中心区域(J.A. Lindsay等人,《分子微生物学》29:527 - 543,1998)。同一多位点酶电泳类型、随机扩增多态性DNA类型和核糖体类型的密切相关菌株RF120不包含该岛,这意味着该元件是可移动的,并且最近发生了插入/缺失事件。通过等位基因替换构建了金黄色葡萄球菌菌株RF122的TSST和TSST/SEC缺陷突变体。通过野生型菌株以及tst和sec-bovine等位基因替换突变体的培养上清液进行的体外牛Vβ特异性淋巴细胞扩增分析表明,TSST刺激BTB13特异性T细胞,而SEC-bovine刺激BTB93特异性T细胞。这表明SaPIbov的存在可能有助于调节牛的免疫反应。

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