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表皮葡萄球菌黏液产生抗原标志物的鉴定

Identification of an antigenic marker of slime production for Staphylococcus epidermidis.

作者信息

Christensen G D, Barker L P, Mawhinney T P, Baddour L M, Simpson W A

机构信息

Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, Missouri 65201.

出版信息

Infect Immun. 1990 Sep;58(9):2906-11. doi: 10.1128/iai.58.9.2906-2911.1990.

Abstract

The pathogenic Staphylococcus epidermidis strain RP62A (ATCC 35984) adheres to smooth surfaces by forming a tenacious bacterial film known as slime. The mechanism of slime production is not known; however, workers in the laboratory of G. Pier (Harvard Medical School, Boston, Mass.) have isolated from RP62A a galactose-rich capsular polysaccharide adhesin (CPA) which mediates the attachment of the organism to smooth surfaces. We have obtained two daughter strains from RP62A that no longer produce slime. One daughter strain, H4A, was obtained by selection for a spontaneous variant; the other strain, HAM892, was obtained by treating growing cultures of RP62A with acriflavin. Using an antiserum generated against whole cells of RP62A, we have examined lysozyme-lysostaphin digests of RP62A, H4A, and HAM892 by double immunodiffusion. The two strains that no longer produced slime no longer produced a particular antigen, which we refer to as the slime-associated antigen (SAA). SAA was also produced by unrelated strains of slime-producing S. epidermidis. SAA was heat and protease stable, had a molecular weight of greater than 50,000, and could be partially purified by chromatographing trypsin-digested material over a Sephadex G-200 column. Chemical analysis of partially purified SAA by gas-liquid chromatography found SAA to be glucose rich (59%) and galactose poor (1.4%). This analysis chemically distinguished SAA from CPA. When tested together by double immunodiffusion with anti-RP62A and anti-CPA antisera, partially purified SAA did not cross-react with CPA. Kinetic studies suggested that SAA is a marker for surface accumulation whereas CPA mediates initial adherence.

摘要

致病性表皮葡萄球菌菌株RP62A(ATCC 35984)通过形成一种称为黏液的坚韧细菌膜附着在光滑表面上。黏液产生的机制尚不清楚;然而,G. Pier(哈佛医学院,马萨诸塞州波士顿)实验室的研究人员从RP62A中分离出一种富含半乳糖的荚膜多糖黏附素(CPA),它介导该生物体附着在光滑表面上。我们从RP62A获得了两个不再产生黏液的子代菌株。一个子代菌株H4A是通过选择自发变体获得的;另一个菌株HAM892是通过用吖啶黄素处理RP62A的生长培养物获得的。使用针对RP62A全细胞产生的抗血清,我们通过双向免疫扩散检查了RP62A、H4A和HAM892的溶菌酶 - 溶葡萄球菌素消化物。这两个不再产生黏液的菌株不再产生一种特定抗原,我们将其称为黏液相关抗原(SAA)。产生黏液的表皮葡萄球菌的无关菌株也产生SAA。SAA对热和蛋白酶稳定,分子量大于50,000,并且可以通过在Sephadex G - 200柱上对胰蛋白酶消化的材料进行色谱分离来部分纯化。通过气 - 液色谱对部分纯化的SAA进行化学分析发现SAA富含葡萄糖(59%)且半乳糖含量低(1.4%)。该分析在化学上区分了SAA和CPA。当与抗RP62A和抗CPA抗血清一起通过双向免疫扩散测试时,部分纯化的SAA与CPA不发生交叉反应。动力学研究表明,SAA是表面积累的标志物,而CPA介导初始黏附。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a80/313585/1819ecb78587/iai00057-0194-a.jpg

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