痤疮杆菌是寻常痤疮的机会致病菌。C.痤疮产生自诱导物-2(AI-2),一种用于通信的信号分子,称为群体感应(QS)。在痤疮杆菌中,据报道,QS上调生物膜形成,导致对杀菌剂的抗性。在这项研究中,我们分析了类肝素如何影响机会病原体痤疮杆菌的QS和生物膜形成。我们还验证了类肝素是否会抑制生物膜形成并增强杀菌剂4-异丙基-3-甲基苯酚(IPMP)对抗痤疮梭菌生物膜的功效。我们使用哈氏弧菌ATCCBBA-1121进行了AI-2生物测定。类肝素在0.003-0.005%的浓度下表现出对AI-2的抑制活性,提示AI-2类似物来源的或痤疮梭菌培养上清液来源的AI-2活性的抑制。为了评估类肝素如何抑制痤疮梭菌的生物膜形成,我们在96孔板中完成了生物膜测定。我们还评估了IPMP对使用或不使用类肝素制备的痤疮梭菌生物膜的杀菌活性。类肝素抑制痤疮梭菌生物膜形成,并且在类肝素介导的生物膜形成抑制后,IPMP杀菌效力增加。在这项研究中,我们澄清了类肝素抑制痤疮丙酸杆菌的AI-2介导的QS,从而抑制生物膜的形成和增加IPMP杀菌效力,可能抑制寻常痤疮。
Cutibacterium acnes is an opportunistic pathogen in acne vulgaris. C. acnes produces autoinducer-2 (AI-2), a signaling molecule used for communication known as quorum sensing (QS). In C. acnes, QS reportedly upregulates biofilm formation leading to resistance against bactericidal agents. In this study, we analyzed how
heparinoid affected QS and biofilm formation of the opportunistic pathogen C. acnes. We also verified whether
heparinoid would suppress biofilm formation and enhance the efficacy of the bactericidal agent 4-isopropyl-3-methylphenol (IPMP) against C. acnes biofilms. We ran an AI-2 bioassay using Vibrio harveyi ATCC BBA-1121.
Heparinoid exhibited inhibitory activity against AI-2 at concentrations of 0.003-0.005%, suggesting an AI-2 analog-derived or C. acnes culture supernatant-derived inhibition of the AI-2 activity. To evaluate how
heparinoid suppresses biofilm formation in C. acnes, we completed a biofilm assay in 96-well plates. We also evaluated the bactericidal activity of IPMP against the C. acnes biofilm prepared with or without heparinoid.
Heparinoid inhibited C. acnes biofilm formation and IPMP bactericidal efficacy increased upon
heparinoid-mediated suppression of biofilm formation. In this study, we clarified that heparinoid inhibits the AI-2-mediated QS of C. acnes, thereby suppressing biofilm formation and increasing IPMP bactericidal efficacy, potentially suppressing acne vulgaris.