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胸膜肺炎放线杆菌 5 型荚膜多糖的抗生物膜活性。

Antibiofilm activity of Actinobacillus pleuropneumoniae serotype 5 capsular polysaccharide.

机构信息

Department of Oral Biology, New Jersey Dental School, Newark, New Jersey, USA.

出版信息

PLoS One. 2013 May 14;8(5):e63844. doi: 10.1371/journal.pone.0063844. Print 2013.

Abstract

Cell-free extracts isolated from colony biofilms of Actinobacillus pleuropneumoniae serotype 5 were found to inhibit biofilm formation by Staphylococcus aureus, S. epidermidis and Aggregatibacter actinomycetemcomitans, but not by A. pleuropneumoniae serotype 5 itself, in a 96-well microtiter plate assay. Physical and chemical analyses indicated that the antibiofilm activity in the extract was due to high-molecular-weight polysaccharide. Extracts isolated from a mutant strain deficient in the production of serotype 5 capsular polysaccharide did not exhibit antibiofilm activity. A plasmid harboring the serotype 5 capsule genes restored the antibiofilm activity in the mutant extract. Purified serotype 5 capsular polysaccharide also exhibited antibiofilm activity against S. aureus. A. pleuropneumoniae wild-type extracts did not inhibit S. aureus growth, but did inhibit S. aureus intercellular adhesion and binding of S. aureus cells to stainless steel surfaces. Furthermore, polystyrene surfaces coated with A. pleuropneumoniae wild-type extracts, but not with capsule-mutant extracts, resisted S. aureus biofilm formation. Our findings suggest that the A. pleuropneumoniae serotype 5 capsule inhibits cell-to-cell and cell-to-surface interactions of other bacteria. A. pleuropneumoniae serotype 5 capsular polysaccharide is one of a growing number of bacterial polysaccharides that exhibit broad-spectrum, nonbiocidal antibiofilm activity. Future studies on these antibiofilm polysaccharides may uncover novel functions for bacterial polysaccharides in nature, and may lead to the development of new classes of antibiofilm agents for industrial and clinical applications.

摘要

从胸膜肺炎放线杆菌 5 型菌落在菌落生物膜中分离出的无细胞提取物被发现可抑制金黄色葡萄球菌、表皮葡萄球菌和伴放线放线杆菌的生物膜形成,但不能抑制 5 型胸膜肺炎放线杆菌自身的生物膜形成,这是在 96 孔微量滴定板测定中发现的。物理和化学分析表明,提取物中的抗生物膜活性是由于高分子量多糖所致。从缺乏 5 型荚膜多糖产生的突变株中分离出的提取物没有表现出抗生物膜活性。携带 5 型荚膜基因的质粒恢复了突变体提取物中的抗生物膜活性。纯化的 5 型荚膜多糖也对金黄色葡萄球菌表现出抗生物膜活性。胸膜肺炎放线杆菌野生型提取物不会抑制金黄色葡萄球菌的生长,但会抑制金黄色葡萄球菌的细胞间粘附和金黄色葡萄球菌细胞与不锈钢表面的结合。此外,用胸膜肺炎放线杆菌野生型提取物涂覆的聚苯乙烯表面,但不是用荚膜突变体提取物涂覆的表面,可抵抗金黄色葡萄球菌生物膜的形成。我们的研究结果表明,胸膜肺炎放线杆菌 5 型荚膜抑制了其他细菌的细胞间和细胞与表面的相互作用。胸膜肺炎放线杆菌 5 型荚膜多糖是越来越多表现出广谱、非杀菌性抗生物膜活性的细菌多糖之一。对这些抗生物膜多糖的进一步研究可能揭示细菌多糖在自然界中的新功能,并可能导致开发用于工业和临床应用的新型抗生物膜剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8097/3653790/9ce19ad85135/pone.0063844.g001.jpg

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