Shanks Robert M Q, Donegan Niles P, Graber Martha L, Buckingham Sarah E, Zegans Michael E, Cheung Ambrose L, O'Toole George A
Department of Microbiology and Immunology, Dartmouth Medical School, Hanover, New Hampshire 03755, USA.
Infect Immun. 2005 Aug;73(8):4596-606. doi: 10.1128/IAI.73.8.4596-4606.2005.
Heparin, known for its anticoagulant activity, is commonly used in catheter locks. Staphylococcus aureus, a versatile human and animal pathogen, is commonly associated with catheter-related bloodstream infections and has evolved a number of mechanisms through which it adheres to biotic and abiotic surfaces. We demonstrate that heparin increased biofilm formation by several S. aureus strains. Surface coverage and the kinetics of biofilm formation were stimulated, but primary attachment to the surface was not affected. Heparin increased S. aureus cell-cell interactions in a protein synthesis-dependent manner. The addition of heparin rescued biofilm formation of hla, ica, and sarA mutants. Our data further suggest that heparin stimulation of biofilm formation occurs neither through an increase in sigB activity nor through an increase in polysaccharide intracellular adhesin levels. These finding suggests that heparin stimulates S. aureus biofilm formation via a novel pathway.
肝素以其抗凝活性而闻名，常用于导管锁中。金黄色葡萄球菌是一种广泛存在于人和动物体内的病原体，通常与导管相关的血流感染有关，并且已经进化出多种机制来使其粘附在生物和非生物表面。我们证明，肝素可增加几种金黄色葡萄球菌菌株的生物膜形成。表面覆盖率和生物膜形成动力学受到刺激，但对表面的初始附着不受影响。肝素以蛋白质合成依赖的方式增加金黄色葡萄球菌的细胞间相互作用。添加肝素可挽救hla、ica和sarA突变体的生物膜形成。我们的数据进一步表明，肝素对生物膜形成的刺激既不是通过增加sigB活性，也不是通过增加多糖细胞内粘附素水平来实现的。这些发现表明，肝素通过一条新途径刺激金黄色葡萄球菌生物膜的形成。
