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首页> 美国卫生研究院文献>Microbiology >Arginine deiminase inhibits Porphyromonas gingivalis surface attachment
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Arginine deiminase inhibits Porphyromonas gingivalis surface attachment

机译：精氨酸脱亚氨酶抑制牙龈卟啉单胞菌表面附着

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摘要

The oral cavity is host to a complex microbial community whose maintenance depends on an array of cell-to-cell interactions and communication networks, with little known regarding the nature of the signals or mechanisms by which they are sensed and transmitted. Determining the signals that control attachment, biofilm development and outgrowth of oral pathogens is fundamental to understanding pathogenic biofilm development. We have previously identified a secreted arginine deiminase (ADI) produced by Streptococcus intermedius that inhibited biofilm development of the commensal pathogen Porphyromonas gingivalis through downregulation of genes encoding the major (fimA) and minor (mfa1) fimbriae, both of which are required for proper biofilm development. Here we report that this inhibitory effect is dependent on enzymic activity. We have successfully cloned, expressed and defined the conditions to ensure that ADI from S. intermedius is enzymically active. Along with the cloning of the wild-type allele, we have created a catalytic mutant (ADIC399S), in which the resulting protein is not able to catalyse the hydrolysis of l-arginine to l-citrulline. P. gingivalis is insensitive to the ADIC399S catalytic mutant, demonstrating that enzymic activity is required for the effects of ADI on biofilm formation. Biofilm formation is absent under l-arginine-deplete conditions, and can be recovered by the addition of the amino acid. Taken together, the results indicate that arginine is an important signal that directs biofilm formation by this anaerobe. Based on our findings, we postulate that ADI functions to reduce arginine levels and, by a yet to be identified mechanism, signals P. gingivalis to alter biofilm development. ADI release from the streptococcal cell and its cross-genera effects are important findings in understanding the nature of inter-bacterial signalling and biofilm-mediated diseases of the oral cavity.
机译：口腔是一个复杂的微生物群落的宿主，该微生物群落的维持取决于一系列细胞间相互作用和通信网络，对其信号和机制的感知和传播的性质知之甚少。确定控制口腔病原体附着，生物膜发育和生长的信号是了解病原性生物膜发育的基础。我们之前已经鉴定出由中间链球菌产生的一种分泌型精氨酸脱亚氨酶（ADI），该蛋白通过下调编码主要（fimA）和次要（mfa1）菌毛的基因来抑制共生病原体牙龈卟啉单胞菌的生物膜发育，而这两个基因都是正常生物膜所必需的。发展。在这里我们报道这种抑制作用取决于酶活性。我们已经成功克隆，表达和定义了条件，以确保来自中间链球菌的ADI具有酶活性。除了野生型等位基因的克隆外，我们还创建了一个催化突变体（ADIC399S），其中得到的蛋白质无法催化L-精氨酸水解为L-瓜氨酸。牙龈卟啉单胞菌对ADIC399S催化突变体不敏感，表明ADI对生物膜形成的作用需要酶活性。在缺少1-精氨酸的条件下不存在生物膜形成，并且可以通过添加氨基酸来恢复。两者合计，结果表明精氨酸是指导该厌氧菌形成生物膜的重要信号。根据我们的发现，我们推测ADI可以降低精氨酸水平，并通过尚未确定的机制向牙龈卟啉单胞菌发出信号来改变生物膜的发育。 ADI从链球菌细胞中释放及其跨年龄的影响是了解细菌间信号传导和生物膜介导的口腔疾病的性质的重要发现。

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