The formation of biofilms by bacteria is of great significance because it involves many physiological changes that serve to protect the cells from various stresses. One of the best-known biofilm-specific properties of bacteria is that bacteria that grow in biofilms are generally more resistant to antibiotics than their planktonic counterparts. In a previous study, osmoregulated periplasmic glucans (OPGs), catalyzed by the opgGH operon, were identified and found to function in Rcs signalling in Yersinia enterocolitica. In this study, the possible contribution of OPGs to antimicrobial resistance of Y. enterocolitica biofilms were investigated, and the results showed that OPGs, especially when overexpressed, conferred a high level of biofilm resistance to two different classes of antibiotics onto Y. enterocolitica. Subsequent analysis revealed that OPGs regulated the biofilm architecture in Y. enterocolitica by promoting the bacteria to form large cell aggregates. Moreover, the opgGH genes in biofilms showed higher expression than in planktonic cultures. OPGs were required to induce the expression of genes related to flagella, extracellular polysaccharide, and c-di-GMP biosynthesis in Y. enterocolitica biofilms and this effect was more significant when OPGs were overproduced. The current investigation showed an extension in the biological role of OPGs in Y. enterocolitica and provided a strong theoretical basis to further study this resistance mechanism at the molecular level to identify new drug targets or disinfectants for the treatment of infections caused by Y. enterocolitica within biofilms.

细菌形成生物膜具有重要意义，因为它涉及许多生理变化，这些变化可保护细胞免受各种压力。细菌最着名的生物膜特有特性之一是，在生物膜中生长的细菌通常比浮游性细菌对抗生素更具抵抗力。在先前的研究中，被opgGH操纵子催化的渗透性周质葡聚糖（OPGs）被鉴定出并在小肠结肠炎耶尔森氏菌的Rcs信号传导中起作用。在这项研究中，OPGs对小肠结肠炎耶尔森氏菌耐药性的可能贡献对生物膜进行了研究，结果表明，OPGs，尤其是在过度表达时，对小肠结肠炎耶尔森氏菌赋予了高水平的生物膜对两种不同类型抗生素的抗性。随后的分析表明，OPG通过促进细菌形成大细胞聚集体来调节小肠结肠炎耶尔森菌的生物膜结构。此外，生物膜中的opgGH基因显示出比浮游培养物中更高的表达。需要OPG诱导小肠结肠炎耶尔森氏菌中鞭毛，细胞外多糖和c-di-GMP生物合成相关基因的表达生物膜，而OPG过度生产时，这种影响更为明显。目前的调查显示，在OPGs的生物学作用延长小肠结肠炎耶尔森菌，并提供了强大的理论基础上，进一步研究在分子水平上该阻力机制，以确定引起感染的治疗新的药物靶标或消毒剂小肠结肠炎耶尔森菌内生物膜。