Valle Jaione, Da Re Sandra, Henry Nelly, Fontaine Thierry, Balestrino Damien, Latour-Lambert Patricia, Ghigo Jean-Marc
Groupe de Génétique des Biofilms, Centre National de la Recherche Scientifique (CNRS), Unité de Recherche Associée 2172, and Unité des Aspergillus, Institut Pasteur, 25 Rue du Dr. Roux, 75724 Paris Cedex 15, France.
Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12558-63. doi: 10.1073/pnas.0605399103. Epub 2006 Aug 7.
The development of surface-attached biofilm bacterial communities is considered an important source of nosocomial infections. Recently, bacterial interference via signaling molecules and surface active compounds was shown to antagonize biofilm formation, suggesting that nonantibiotic molecules produced during competitive interactions between bacteria could be used for biofilm reduction. Hence, a better understanding of commensal/pathogen interactions within bacterial community could lead to an improved control of exogenous pathogens. To reveal adhesion or growth-related bacterial interference, we investigated interactions between uropathogenic and commensal Escherichia coli in mixed in vitro biofilms. We demonstrate here that the uropathogenic strain CFT073 and all E. coli expressing group II capsules release into their environment a soluble polysaccharide that induces physicochemical surface alterations, which prevent biofilm formation by a wide range of Gram-positive and Gram-negative bacteria. We show that the treatment of abiotic surfaces with group II capsular polysaccharides drastically reduces both initial adhesion and biofilm development by important nosocomial pathogens. These findings identify capsular polymers as antiadhesion bacterial interference molecules, which may prove to be of significance in the design of new strategies to limit biofilm formation on medical in dwelling devices.
表面附着的生物膜细菌群落的发展被认为是医院感染的一个重要来源。最近,通过信号分子和表面活性化合物进行的细菌干扰被证明可拮抗生物膜形成,这表明细菌之间竞争性相互作用过程中产生的非抗生素分子可用于减少生物膜。因此,更好地理解细菌群落内共生菌/病原体的相互作用可能会改善对外源性病原体的控制。为了揭示与黏附或生长相关的细菌干扰,我们研究了尿路致病性大肠杆菌和共生大肠杆菌在体外混合生物膜中的相互作用。我们在此证明,尿路致病性菌株CFT073以及所有表达II组荚膜的大肠杆菌会向其周围环境释放一种可溶性多糖,这种多糖会引起物理化学表面变化,从而阻止多种革兰氏阳性和革兰氏阴性细菌形成生物膜。我们表明,用II组荚膜多糖处理非生物表面可显著减少重要医院病原体的初始黏附和生物膜形成。这些发现将荚膜聚合物确定为抗黏附细菌干扰分子,这可能在设计限制医疗植入设备上生物膜形成的新策略方面具有重要意义。