Clinical Laboratory Center, People's Hospital of Xinjiang Uygur Autonomous Region, Wulumuqi, Xinjiang, China (mainland).
Med Sci Monit. 2023 Sep 9;29:e940704. doi: 10.12659/MSM.940704.
BACKGROUND Previous research reported that the resistance mechanism of Acinetobacter baumannii resistance to tigecycline was mainly related to the overexpression of the AdeABC efflux pump system. Biofilm formation is a notable pathogenesis of A. baumannii infections and antibiotic resistance. Our study explores the latent relevance of biofilm-associated genes and efflux pump genes in A. baumannii tigecycline resistance. MATERIAL AND METHODS A total of 78 clinical samples were collected from October 2018 to October 2019. Seventy-two clinically isolated A. baumannii strains were divided into a tigecycline-resistant Acinetobacter baumannii (TR-AN) group and tigecycline-sensitive Acinetobacter baumannii (TS-AN) group by tigecycline minimum inhibitory concentration tests. The biofilm formation of the 2 groups was observed using crystal violet staining. Furthermore, biofilm-related genes and efflux pump genes were analyzed by RT-PCR. RESULTS The biofilm-forming rate of the TR-AN group was 82.2%, and that of the TS-AN group was 14.8%. The biofilm synthesis gene bfs was 91.3% positive in the TR-AN group, significantly higher than in the TS-AN group at the transcription level (P<0.05). The minimum inhibitory concentration of tigecycline was higher in the TR-AN group with biofilm formation than in the TR-AN group without biofilm formation (P<0.05). The efflux pump AdeB gene was 95.2% positive in the TR-AN group with biofilm formation and 38.7% positive in the TR-AN group without biofilm formation. CONCLUSIONS The biofilm formation of A. baumannii may be positively related to tigecycline resistance ability because of the co-expression of the bfs gene and the AdeB efflux pump gene. The enhanced transcription level of bfs and AdeB promotes biofilm formation to improve the resistance of A. baumannii to tigecycline.
先前的研究表明，鲍曼不动杆菌对替加环素的耐药机制主要与 AdeABC 外排泵系统的过度表达有关。生物膜形成是鲍曼不动杆菌感染和抗生素耐药性的一个显著发病机制。本研究探讨了生物膜相关基因和外排泵基因与鲍曼不动杆菌替加环素耐药性之间的潜在相关性。
共收集了 2018 年 10 月至 2019 年 10 月期间的 78 份临床样本。72 株临床分离的鲍曼不动杆菌菌株根据替加环素最低抑菌浓度试验分为替加环素耐药鲍曼不动杆菌（TR-AN）组和替加环素敏感鲍曼不动杆菌（TS-AN）组。通过结晶紫染色观察两组的生物膜形成情况。此外，通过 RT-PCR 分析生物膜相关基因和外排泵基因。
TR-AN 组的生物膜形成率为 82.2%，TS-AN 组为 14.8%。TR-AN 组的生物膜合成基因 bfs 在转录水平上的阳性率为 91.3%，明显高于 TS-AN 组（P<0.05）。具有生物膜形成的 TR-AN 组的替加环素最小抑菌浓度高于无生物膜形成的 TR-AN 组（P<0.05）。具有生物膜形成的 TR-AN 组的外排泵 AdeB 基因阳性率为 95.2%，无生物膜形成的 TR-AN 组为 38.7%。
鲍曼不动杆菌的生物膜形成可能与替加环素耐药能力呈正相关，这是由于 bfs 基因和 AdeB 外排泵基因的共表达所致。bfs 和 AdeB 的转录水平增强促进了生物膜的形成，从而提高了鲍曼不动杆菌对替加环素的耐药性。
