Botany and Microbiology Department, Faculty of Science, Alexandria University, Alexandria, Egypt.
Pharmacognosy Department, Faculty of Pharmacy, Mansoura University, El Mansûra, 35516, Egypt.
World J Microbiol Biotechnol. 2022 Jul 8;38(9):156. doi: 10.1007/s11274-022-03337-x.
The number of deaths caused by multidrug-resistant Pseudomonas aeruginosa has risen in the recent decade. The development of quorum sensing inhibition (QSI) is a promising approach for controlling Pseudomonas infection. Therefore, this study mainly aimed to investigate how a plant-source material inhibits QSI to produce an antipathogenic effect for fighting microbial infections. The QSI effect of Trigonella stellata was assessed by using Chromobacterium violaceum ATCC 12472 reporter strain. Trigonella stellata exhibited high QSI activity, and an ethanolic extract of T. stellata was prepared for phytochemical isolation of the most active QSI compound. Nine pure compounds were isolated and identified as kaempferitrin (1), soyasaponin I (2), β-sitosterol-3-O-glucoside (3), dihydromelilotoside (4), astrasikokioside I (5), methyl dihydromelilotoside (6), (3R, 4S)-4, 2', 4'-trihydroxy-7-methoxy-4'-O-β-D-glucopyranosylisoflavan (7), (3S, 4R)-4, 2', 4'-trihydroxy-7-methoxyisoflavan (8, TMF), and (+)-D-pinitol (9). These compounds were screened against C. violaceum ATCC 12472, and TMF exhibited a potent QSI. The effect of TMF at sub-minimum inhibitory concentrations (MICs) was assessed against P. aeruginosa virulence factors, including biofilm, pyocyanin formation protease and hemolysin activity. TMF induced significant elimination of QS-associated virulence behavior. In addition, TMF at sub-MICs significantly reduced the relative expression of lasI, lasR, rhlI, and rhlR compared with that in untreated cells. Furthermore, molecular docking was performed to predict structural basis of the QSI activity of TMF. The study demonstrated the importance of T. stellata as a signal modulator and inhibitor of P. aeruginosa pathogenesis.
近十年来，由多药耐药铜绿假单胞菌引起的死亡人数有所增加。群体感应抑制（QSI）的发展是控制铜绿假单胞菌感染的一种很有前途的方法。因此，本研究主要旨在探讨植物源材料如何抑制 QSI 以产生抗病原体作用来对抗微生物感染。采用 Chromobacterium violaceum ATCC 12472 报告菌株评估了紫云英的 QSI 作用。紫云英表现出很高的 QSI 活性，并用紫云英的乙醇提取物制备了最活跃的 QSI 化合物的植物化学分离物。分离并鉴定了 9 种纯化合物，分别为山奈酚（1）、大豆皂甙 I（2）、β-谷甾醇-3-O-葡萄糖苷（3）、二氢麦角甾苷（4）、阿斯特拉西考甙 I（5）、甲基二氢麦角甾苷（6）、(3R, 4S)-4,2',4'-三羟基-7-甲氧基-4'-O-β-D-吡喃葡萄糖基异黄酮（7）、(3S, 4R)-4,2',4'-三羟基-7-甲氧基异黄酮（8，TMF）和（+）-D-松醇（9）。这些化合物对 C. violaceum ATCC 12472 进行了筛选，TMF 表现出很强的 QSI 活性。在亚最低抑菌浓度（MIC）下评估了 TMF 对铜绿假单胞菌毒力因子的影响，包括生物膜、绿脓菌素形成蛋白酶和溶血素活性。TMF 诱导 QS 相关毒力行为的显著消除。此外，与未经处理的细胞相比，TMF 在亚 MICs 下显著降低了 lasI、lasR、rhlI 和 rhlR 的相对表达。此外，还进行了分子对接以预测 TMF 的 QSI 活性的结构基础。该研究表明，紫云英作为铜绿假单胞菌发病机制的信号调节剂和抑制剂具有重要意义。
