Inhibition of polysaccharide synthesis by the sinR orthologue PGN_0088 is indirectly associated with the penetration of Porphyromonas gingivalis biofilms by macrolide antibiotics.
Inhibition of polysaccharide synthesis by the sinR orthologue PGN_0088 is indirectly associated with the penetration of Porphyromonas gingivalis biofilms by macrolide antibiotics.
复制标题
sinR 直系同源物 PGN_0088 对多糖合成的抑制与大环内酯类抗生素对牙龈卟啉单胞菌生物膜的渗透间接相关。
DOI：
10.1099/mic.0.000013
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发表时间：
2015
期刊：
影响因子：
1.5
通讯作者：
Hayashi M
中科院分区：
文献类型：
--
作者：
Yamamoto R;Noiri Y;Yamaguchi M;Asahi Y;Maezono H;Ebisu S;Hayashi M
微生物通常附着在表面，聚集在自产的胞外聚合物（EPS）中并生活在生物膜中。牙周炎是一种严重的口腔感染，是由牙龈卟啉单胞菌形成的生物膜引起的。EPS作为一种屏障，保护生物膜形成细胞免受应激源的影响，包括宿主免疫细胞和抗菌剂诱导的应激源。因此，旨在杀死此类微生物的药物不能用于治疗生物膜感染。本课题组前期研究表明，阿奇霉素和红霉素的亚最小抑菌浓度（subminimal inhibitory concentration，subMIC）可降低P。牙龈生物膜。此外，我们证明了枯草芽孢杆菌同源物（PGN_0088）抑制了P.牙龈生物膜。在这里，我们从P. gingivalisATCC 33277的结果，并揭示突变体的EPS中碳水化合物丰度的增加导致AZM和ERY通过EPS的浸润速率降低，并因此提高了生物膜对这些大环内酯类的抗性。详细阐明thesinR基因的产物和EPS之间的相互作用，将有助于开发新的方法，针对EPS，以防止和抑制生物膜的形成。
Microbes commonly adhere to surfaces, aggregate in self-produced extracellular polymeric substances (EPS) and live in biofilms. Periodontitis is a serious oral infection that is initiated by the formation of biofilms byPorphyromonas gingivalis. EPS act as a barrier that protects biofilm-forming cells against sources of stress, including those induced by host immune cells and antimicrobial agents. Therefore, drugs intended to kill such micro-organisms cannot be used for the treatment of biofilm infections. Our previous studies revealed that subminimal inhibitory concentrations (subMIC) of two macrolide antibiotics (azithromycin, AZM and erythromycin, ERY) reducedP. gingivalisbiofilms. Furthermore, we demonstrated that theBacillus subtilis sinRorthologue (PGN_0088) inhibits the synthesis of carbohydrates that are components of EPS inP. gingivalisbiofilms. Here, we constructed a novelsinRmutant fromP. gingivalisATCC 33277 and reveal that the increased abundance of carbohydrate in EPS of the mutant led to a reduced infiltration rate of AZM and ERY through EPS, and consequently elevated biofilm resistance to these macrolides. Detailed elucidation of the interaction between the product of thesinRgene and EPS will assist in the development of novel approaches that target EPS to prevent and inhibit the formation of biofilms.