McCourt Jennifer, O'Halloran Dara P, McCarthy Hannah, O'Gara James P, Geoghegan Joan A
Department of Microbiology, Moyne Institute of Preventive Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland.
FEMS Microbiol Lett. 2014 Apr;353(2):157-64. doi: 10.1111/1574-6968.12424. Epub 2014 Apr 10.
Community-associated methicillin-resistant Staphylococcus aureus of the USA300 lineage is emerging as an important cause of medical device-related infection. However, few factors required for biofilm accumulation by USA300 strains have been identified, and the processes involved are poorly understood. Here, we identify S. aureus proteins required for the USA300 isolate LAC to form biofilm. A mutant with a deletion of the fnbA and fnbB genes did not express the fibronectin-binding proteins FnBPA and FnBPB and lacked the ability to adhere to fibronectin or to form biofilm. Biofilm formation by the mutant LAC∆fnbAfnbB could be restored by expression of FnBPA or FnBPB from a plasmid demonstrating that both of these proteins can mediate biofilm formation when expressed by LAC. Expression of FnBPA and FnBPB increased bacterial aggregation suggesting that fibronectin-binding proteins can promote the accumulation phase of biofilm. Loss of fibronectin-binding proteins reduced the initial adherence of bacteria, indicating that these proteins are also involved in primary attachment. In summary, these findings improve our understanding of biofilm formation by the USA300 strain LAC by demonstrating that the fibronectin-binding proteins are required.
社区获得性耐甲氧西林金黄色葡萄球菌USA300菌系正逐渐成为医疗器械相关感染的重要原因。然而,目前已确定的USA300菌株形成生物膜所需的因素较少,且对其中涉及的过程了解甚少。在此,我们确定了USA300分离株LAC形成生物膜所需的金黄色葡萄球菌蛋白。缺失fnbA和fnbB基因的突变体不表达纤连蛋白结合蛋白FnBPA和FnBPB,并且缺乏黏附纤连蛋白或形成生物膜的能力。突变体LAC∆fnbAfnbB的生物膜形成可通过从质粒表达FnBPA或FnBPB来恢复,这表明当由LAC表达时,这两种蛋白均可介导生物膜形成。FnBPA和FnBPB的表达增加了细菌聚集,表明纤连蛋白结合蛋白可促进生物膜的聚集阶段。纤连蛋白结合蛋白的缺失降低了细菌的初始黏附,表明这些蛋白也参与了初始附着。总之,这些发现通过证明纤连蛋白结合蛋白是必需的,提高了我们对USA300菌株LAC形成生物膜的理解。