Li Ying, Cao Sanjie, Zhang Luhua, Lau Gee W, Wen Yiping, Wu Rui, Zhao Qin, Huang Xiaobo, Yan Qigui, Huang Yong, Wen Xintian
Research Center of Swine Diseases, College of Veterinary Medicine, Sichuan Agricultural University Chengdu, China.
Research Center of Swine Diseases, College of Veterinary Medicine, Sichuan Agricultural UniversityChengdu, China; Department of Pathobiology, University of Illinois at Urbana-ChampaignUrbana, IL, USA.
Front Microbiol. 2016 Oct 24;7:1618. doi: 10.3389/fmicb.2016.01618. eCollection 2016.
is the etiologic agent of porcine contagious pleuropneumonia, a significant disease that causes serious economic losses to the swine industry worldwide. Persistent infections caused by bacterial biofilms are recalcitrant to treat because of the particular drug resistance of biofilm-dwelling cells. TolC, a key component of multidrug efflux pumps, are responsible for multidrug resistance (MDR) in many Gram-negative bacteria. In this study, we identified two TolC-like proteins, TolC1 and TolC2, in Deletion of , but not , caused a significant reduction in biofilm formation, as well as increased drug sensitivity of both planktonic and biofilm cells. The genetic-complementation of the mutation restored the competent biofilm and drug resistance. Besides, biofilm formation was inhibited and drug sensitivity was increased by the addition of phenylalanine-arginine beta-naphthylamide (PAβN), a well-known efflux pump inhibitor (EPI), suggesting a role for EPI in antibacterial strategies toward drug tolerance of . Taken together, TolC1 is required for biofilm formation and is a part of the MDR machinery of both planktonic and biofilm cells, which could supplement therapeutic strategies for resistant bacteria and biofilm-related infections of clinical isolate SC1516.
是猪传染性胸膜肺炎的病原体，这是一种对全球养猪业造成严重经济损失的重要疾病。细菌生物膜引起的持续性感染难以治疗，因为生物膜内细胞具有特殊的耐药性。TolC是多药外排泵的关键组成部分，在许多革兰氏阴性细菌中导致多药耐药（MDR）。在本研究中，我们在中鉴定出两种类TolC蛋白，即TolC1和TolC2。缺失而非缺失导致生物膜形成显著减少，以及浮游细胞和生物膜细胞的药物敏感性增加。突变的基因互补恢复了正常的生物膜和耐药性。此外，添加著名的外排泵抑制剂（EPI）苯丙氨酸-精氨酸β-萘酰胺（PAβN）可抑制生物膜形成并增加药物敏感性，这表明EPI在针对临床分离株SC1516耐药性的抗菌策略中发挥作用。综上所述，TolC1是生物膜形成所必需的，并且是浮游细胞和生物膜细胞MDR机制的一部分，这可为耐药细菌和临床分离株SC1516生物膜相关感染的治疗策略提供补充。
