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常规抗生素治疗可能诱导产志贺毒素大肠杆菌（Shiga toxin-producing Escherichia coli, STEC）前噬菌体裂解并释放毒素，加剧其临床危害，所以抑制STEC毒素产生及子代噬菌体释放是防控STEC感染的关键。本研究通过体外抑菌实验发现，马齿苋多糖（POP）对大肠杆菌、金黄色葡萄球菌及铜绿假单胞菌均具有抑制作用，对STEC菌株Min27的最小抑菌浓度（MIC）为125 mg/mL。在62.5 mg/mL(1/2MIC)亚抑菌浓度下，POP能显著地减弱STEC Min27的爬行运动能力，并使菌落边缘趋于光滑；同时，细菌对巨噬细胞的黏附数量下降到原来水平的1/100，与对照组相比较；子代Stx噬菌体的效价降低约2个数量级。研究结果表明，POP对STEC具有多重抑制效果，除表现出良好的抑菌能力外，还可干扰其运动、生物被膜形成及黏附等关键毒力表型，并有效抑制Stx噬菌体的裂解释放。因此，POP是一种兼具抗菌活性和抑制水平基因转移潜力的制剂，为STEC感染的防控提供了新思路。
Abstract：Conventional antibiotic treatment may induce the lysis of Shiga toxin producing Escherichia coli(STEC) prophages, thereby triggering toxin release and exacerbating clinical harm. Therefore, inhibiting STEC toxin production and progeny phage release is crucial for the prevention and control of STEC infection. In vitro antibacterial studies revealed that Portulaca oleracea polysaccharide(POP) inhibits E. coli, Staphylococcus aureus, and Pseudomonas aeruginosa, with a minimum inhibitory concentration(MIC) of 125 mg/mL against STEC strain Min27. At the subinhibitory concentration of 62.5 mg/mL(1/2 MIC), POP significantly impaired the swarm motility of STEC Min27, resulting in smoother colony margins. Concurrently, bacterial adhesion to macrophages decreased approximately 100-fold, and the titer of Stx phage progeny was reduced by approximately two orders of magnitude compared to the control group. The findings indicate that POP exerts multiple inhibitory effects on STEC. In addition to exhibiting potent antibacterial activity, it interferes with key virulence phenotypes such as motility, biofilm formation, and adhesion, and effectively inhibits the lytic release of Stx phages. Thus,POP is an agent with both antibacterial activity and the potential to inhibit horizontal gene transfer, providing a novel approach for controlling STEC infection.
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基本信息:
中图分类号:R285
引用信息:
[1]鄢灿,邱琳,蔡思艺,等.马齿苋多糖对产志贺毒素大肠杆菌的毒力影响作用及抑菌效果评价[J].井冈山大学学报(自然科学版),2026,47(03):33-41.
基金信息:
国家自然科学基金项目（32460913）; 江西省自然科学基金面上项目（20232BAB205009,20252BAC240486）; 吉安市自然科学基金项目（20255-061661）
2026-05-10
2026-05-10