Surfactants’ Interplay with Biofilm Development in Staphylococcus and Candida

F. Aonofriesei
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Abstract

The capacity of micro-organisms to form biofilms is a pervasive trait in the microbial realm. For pathogens, biofilm formation serves as a virulence factor facilitating successful host colonization. Simultaneously, infections stemming from biofilm-forming micro-organisms pose significant treatment challenges due to their heightened resistance to antimicrobial agents. Hence, the quest for active compounds capable of impeding microbial biofilm development stands as a pivotal pursuit in biomedical research. This study presents findings concerning the impact of three surfactants, namely, polysorbate 20 (T20), polysorbate 80 (T80), and sodium dodecyl sulfate (SDS), on the initial stage of biofilm development in both Staphylococcus aureus and Candida dubliniensis. In contrast to previous investigations, we conducted a comparative assessment of the biofilm development capacity of these two taxonomically distant groups, predicated on their shared ability to reduce TTC. The common metabolic trait shared by S. aureus and C. dubliniensis in reducing TTC to formazan facilitated a simultaneous evaluation of biofilm development under the influence of surfactants across both groups. Our results revealed that surfactants could impede the development of biofilms in both species by disrupting the initial cell attachment step. The observed effect was contingent upon the concentration and type of compound, with a higher inhibition observed in culture media supplemented with SDS. At maximum concentrations (5%), T20 and T80 significantly curtailed the formation and viability of S. aureus and C. dubliniensis biofilms. Specifically, T20 inhibited biofilm development by 75.36% in S. aureus and 71.18% in C. dubliniensis, while T80 exhibited a slightly lower inhibitory effect, with values ranging between 66.68% (C. dubliniensis) and 65.54% (S. aureus) compared to the controls. Incorporating these two non-toxic surfactants into pharmaceutical formulations could potentially enhance the inhibitory efficacy of selected antimicrobial agents, particularly in external topical applications.
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表面活性剂与葡萄球菌和念珠菌生物膜发展的相互作用
微生物形成生物膜的能力是微生物领域的一个普遍特征。对于病原体来说,生物膜的形成是一种毒力因子,有助于宿主成功定殖。同时,由于生物膜形成微生物对抗菌剂的耐药性较强,它们造成的感染给治疗带来了巨大挑战。因此,在生物医学研究中,寻找能够阻碍微生物生物膜发展的活性化合物是一项至关重要的任务。本研究介绍了聚山梨醇酯 20(T20)、聚山梨醇酯 80(T80)和十二烷基硫酸钠(SDS)这三种表面活性剂对金黄色葡萄球菌和杜布林念珠菌生物膜形成初期的影响。与之前的研究不同,我们对这两个在分类学上相距甚远的类群的生物膜发育能力进行了比较评估,以它们共同的 TTC 还原能力为基础。金黄色葡萄球菌和杜布林杆菌在将四氯化碳还原为甲臢方面具有共同的新陈代谢特征,这有助于同时评估两类细菌在表面活性剂影响下的生物膜形成情况。我们的研究结果表明,表面活性剂可以通过破坏最初的细胞附着步骤来阻碍两种生物膜的形成。观察到的效果取决于化合物的浓度和类型,在添加了 SDS 的培养基中观察到的抑制作用更大。在最高浓度(5%)下,T20 和 T80 能显著抑制金黄色葡萄球菌和杜布林杆菌生物膜的形成和存活。具体来说,与对照组相比,T20 对金黄色葡萄球菌生物膜形成的抑制率为 75.36%,对杜布林杆菌生物膜形成的抑制率为 71.18%,而 T80 的抑制率略低,在 66.68%(杜布林杆菌)和 65.54%(金黄色葡萄球菌)之间。在药物配方中加入这两种无毒表面活性剂有可能提高某些抗菌剂的抑菌效果,特别是在外用局部应用中。
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