Hanna Andrea, Berg Michael, Stout Valerie, Razatos Anneta
Department of Chemical and Materials Engineering. The Molecular and Cellular Biology Program, Arizona State University, Tempe, Arizona 85287, USA.
Appl Environ Microbiol. 2003 Aug;69(8):4474-81. doi: 10.1128/AEM.69.8.4474-4481.2003.
Urinary tract infections are the most common urologic disease in the United States and one of the most common bacterial infections of any organ system. Biofilms persist in the urinary tract and on catheter surfaces because biofilm microorganisms are resistant to host defense mechanisms and antibiotic therapy. The first step in the establishment of biofilm infections is bacterial adhesion; preventing bacterial adhesion represents a promising method of controlling biofilms. Evidence suggests that capsular polysaccharides play a role in adhesion and pathogenicity. This study focuses on the role of physiochemical and specific binding interactions during adhesion of colanic acid exopolysaccharide mutant strains. Bacterial adhesion was evaluated for isogenic uropathogenic Escherichia coli strains that differed in colanic acid expression. The atomic force microscope (AFM) was used to directly measure the reversible physiochemical and specific binding interactions between bacterial strains and various substrates as bacteria initially approach the interface. AFM results indicate that electrostatic interactions were not solely responsible for the repulsive forces between the colanic acid mutant strains and hydrophilic substrates. Moreover, hydrophobic interactions were not found to play a significant role in adhesion of the colanic acid mutant strains. Adhesion was also evaluated by parallel-plate flow cell studies in comparison to AFM force measurements to demonstrate that prolonged incubation times alter bacterial adhesion. Results from this study demonstrate that the capsular polysaccharide colanic acid does not enhance bacterial adhesion but rather blocks the establishment of specific binding as well as time-dependent interactions between uropathogenic E. coli and inert substrates.
在美国,尿路感染是最常见的泌尿系统疾病,也是任何器官系统中最常见的细菌感染之一。生物膜在尿路和导管表面持续存在,因为生物膜微生物对宿主防御机制和抗生素治疗具有抗性。生物膜感染形成的第一步是细菌黏附;防止细菌黏附是控制生物膜的一种有前景的方法。有证据表明,荚膜多糖在黏附和致病性方面发挥作用。本研究聚焦于结肠酸胞外多糖突变株黏附过程中物理化学和特异性结合相互作用的作用。对结肠酸表达不同的同基因尿路致病性大肠杆菌菌株的细菌黏附进行了评估。当细菌最初接近界面时,使用原子力显微镜(AFM)直接测量细菌菌株与各种底物之间可逆的物理化学和特异性结合相互作用。AFM结果表明,静电相互作用并非结肠酸突变株与亲水性底物之间排斥力的唯一原因。此外,未发现疏水相互作用在结肠酸突变株的黏附中起重要作用。与AFM力测量相比,还通过平行平板流动池研究评估了黏附情况,以证明延长孵育时间会改变细菌黏附。本研究结果表明,荚膜多糖结肠酸不会增强细菌黏附,而是会阻断尿路致病性大肠杆菌与惰性底物之间特异性结合以及时间依赖性相互作用的建立。