Food Science and Technology, University of Nebraska, Lincoln, USA.
Curr Microbiol. 2011 May;62(5):1448-54. doi: 10.1007/s00284-011-9882-8. Epub 2011 Feb 4.
Cronobacter sakazakii is an opportunistic pathogen that has been implicated in meningitis, NEC, and sepsis in neonates. Colonization and subsequent infection and invasion of C. sakazakii require that the organism adheres to host cell surfaces. Agents that inhibit or block attachment of the pathogen to epithelial cells could be useful in reducing infections. The goal of this research was to assess the ability of prebiotic galactooligosaccharides (GOS) and polydextrose (PDX) to inhibit adherence of C. sakazakii 4603 to a HEp-2 human cell line. Adherence experiments were performed in the presence or absence of prebiotics using HEp-2 cells grown to confluency on glass coverslips. Prebiotics and bacteria were added and incubated for 3 h. Coverslips were washed, and adherence was determined by cultural and microscopic methods. When measured microscopically or by cultural methods, significant reductions in adherence (56 and 71%, respectively) of C. sakazakii were observed in the presence of GOS (16 mg/ml). Adherence inhibition also occurred (48%) when a GOS-PDX blend (8 mg/ml each) was tested, although PDX by itself had less effect. Similar results were also observed for Caco-2 cells and also for another strain of C. sakazakii (29004). These results suggest that GOS and PDX, alone and in combination, may have an anti-adhesive effect on C. sakazakii and directly inhibit the adherence to gastrointestinal epithelial cells.
阪崎克罗诺杆菌是一种机会致病菌，与新生儿脑膜炎、坏死性小肠结肠炎和败血症有关。该菌的定植以及随后的感染和侵袭需要其黏附于宿主细胞表面。能够抑制或阻断病原体与上皮细胞黏附的药物可能有助于减少感染。本研究旨在评估益生元半乳糖低聚糖（GOS）和聚右旋糖（PDX）抑制阪崎克罗诺杆菌 4603 黏附至 HEp-2 人细胞系的能力。在存在或不存在益生元的情况下，通过在玻璃载玻片上生长至汇合的 HEp-2 细胞进行黏附实验。添加益生元和细菌，并孵育 3 小时。用洗涤缓冲液冲洗载玻片，并通过培养和显微镜方法确定黏附情况。通过显微镜或培养方法测量时，GOS（16mg/ml）存在时，阪崎克罗诺杆菌的黏附（分别为 56%和 71%）显著降低。当测试 GOS-PDX 混合物（各 8mg/ml）时，也发生了黏附抑制（48%），尽管 PDX 本身的作用较小。在 Caco-2 细胞和另一种阪崎克罗诺杆菌（29004）中也观察到了类似的结果。这些结果表明，GOS 和 PDX 单独和联合使用可能对阪崎克罗诺杆菌具有抗黏附作用，并直接抑制其对胃肠道上皮细胞的黏附。
