Fteita Dareen, Musrati Ahmed Ali, Könönen Eija, Ma Xiaochu, Gürsoy Mervi, Peurla Markus, Söderling Eva, Sintim Herman O, Gürsoy Ulvi Kahraman
Department of Periodontology, Institute of Dentistry, University of Turku, FI-20520, Turku, Finland.
Department of Periodontology, Institute of Dentistry, University of Turku, FI-20520, Turku, Finland; Welfare Division, Oral Health Care, City of Turku, Turku, Finland.
Anaerobe. 2017 Dec;48:152-159. doi: 10.1016/j.anaerobe.2017.08.009. Epub 2017 Aug 15.
Biofilm formation and dipeptidyl peptidase IV (DPPIV) enzyme activity contribute to the virulence of oral bacteria, and these virulence factors are partly regulated by quorum sensing signaling system. We recently demonstrated that estradiol regulates growth properties and DPPIV activity of Prevotella intermedia, Prevotella nigrescens, and Prevotella pallens. Here, we examined the DPPIV dependency of biofilm formation of Prevotella aurantiaca. Three strains (two clinical strains AHN 37505 and 37552 and the type strain CCUG 57723) were incubated in three estradiol concentrations (30, 90, and 120 nmol/L). Regulation of DPPIV activity, biofilm and fimbria formation, and coaggregation of bacterial strains were analyzed after incubation with four concentrations (10 nM, 100 nM, 1 μM, 10 μM) of dihydroxy-2,3-pentaedione (DPD), the universal precursor of autoinducer -2 (AI-2), and analogs (ethyl-DPD, butyl-DPD, and isobutyl-DPD) for 24 h. Estradiol enhanced the planktonic growth, coaggregation, and biofilm formation of P. aurantiaca strains. The whole cell extract of AHN 37505 had the highest DPPIV activity, followed by CCUG 57723 and AHN 37552. Inhibition of DPPIV activity with di-isopropylfluorophosphate suppressed the effect of estradiol on biofilm formation. At 100 nM and 10 μM concentrations of DPD, butyl DPD, and isobutyl DPD, biofilm formation of P. aurantiaca was significantly inhibited. Fimbriae formation was enhanced up to concentrations of 100 nM and 1 μM followed by a significant inhibition at higher concentrations of DPD and all analogs. A slight but significant inhibitory effect of DPD and analogs on DPPIV activity was observed. Our results indicate that DPPIV plays a key role in the estradiol-regulated biofilm formation of P. aurantiaca. Quorum sensing autoinducer DPD and C1-alkyl analogs could inhibit biofilm-related virulence of P. aurantiaca.
生物膜形成和二肽基肽酶IV(DPPIV)酶活性有助于口腔细菌的致病性,并且这些致病因素部分受群体感应信号系统调控。我们最近证明,雌二醇可调节中间普氏菌、变黑普氏菌和苍白普氏菌的生长特性及DPPIV活性。在此,我们研究了橙黄普氏菌生物膜形成对DPPIV的依赖性。将三株菌(两株临床菌株AHN 37505和37552以及模式菌株CCUG 57723)在三种雌二醇浓度(30、90和120 nmol/L)下培养。在与四种浓度(10 nM、100 nM、1 μM、10 μM)的二羟基-2,3-戊二酮(DPD,自诱导物-2(AI-2)的通用前体)及其类似物(乙基-DPD、丁基-DPD和异丁基-DPD)孵育24小时后,分析DPPIV活性、生物膜和菌毛形成以及菌株的共聚作用的调节情况。雌二醇增强了橙黄普氏菌菌株的浮游生长、共聚作用和生物膜形成。AHN 37505的全细胞提取物具有最高的DPPIV活性,其次是CCUG 57723和AHN 37552。用二异丙基氟磷酸抑制DPPIV活性可抑制雌二醇对生物膜形成的影响。在100 nM和10 μM浓度的DPD、丁基-DPD和异丁基-DPD下,橙黄普氏菌的生物膜形成受到显著抑制。菌毛形成在浓度高达100 nM和1 μM时增强,随后在更高浓度的DPD和所有类似物作用下受到显著抑制。观察到DPD及其类似物对DPPIV活性有轻微但显著的抑制作用。我们的结果表明,DPPIV在雌二醇调节的橙黄普氏菌生物膜形成中起关键作用。群体感应自诱导物DPD和C1-烷基类似物可抑制橙黄普氏菌与生物膜相关的致病性。