{"title":"Effect of amikacin-humic acid combination on <i>Acinetobacter baumannii</i> biofilm: an <i>in vitro</i> and <i>in silico</i> study.","authors":"Seetha Lakshmi Rajangam, Kakithakara Vajravelu Leela, Manonmoney Jayaraman, Sarvesh Sabarathinam, Manoj Kumar Narasimhan","doi":"10.1080/17460913.2024.2412431","DOIUrl":null,"url":null,"abstract":"<p><p><b>Aim:</b> <i>Acinetobacter baumannii</i> (AB) is a clinically important bacterial pathogen responsible for nosocomial infections. The biofilm-forming capability of these pathogens reduces the antibiotic penetration and its efficacy, thereby complicating the treatment. The current work aims to isolate the most potent biofilm-forming <i>Acinetobacter</i> species from clinical isolates of the patient samples and to evaluate the efficacy of the amikacin-humic acid combination against it.<b>Methods:</b> The combination effect of Amikacin-Humic (AMK-HUM) acid against the highest biofilm-producing <i>A. baumannii</i> SLMK001 was studied via <i>in</i>-<i>vitro</i> (microscopic analysis) and <i>in</i>-<i>silico</i> (Network Pharmacology) analysis.<b>Results:</b> The amikacin-humic acid combination significantly inhibited both the biofilm formation and cell viability of <i>A. baumannii</i> SLMK001. The images observed via Scanning Electron Microscope (SEM) showed a significant decrease in the biofilm matrix. Confocal Laser Scanning Microscope (CLSM) confirmed a reduction of the Z value of its three-dimensional structure. Further, the Network Pharmacology approach supported these experimental findings by identifying the key targets of the amikacin-humic acid combination against the biofilm pathways of <i>A. baumannii</i>.<b>Conclusion:</b> The <i>in-vitro</i> results aligned with the <i>in-silico</i> findings, indicating that the AMK-HUM combination is a promising treatment that significantly activates the key proteins against <i>A. baumannii</i> biofilm formation and pathogenesis.</p>","PeriodicalId":12773,"journal":{"name":"Future microbiology","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Future microbiology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/17460913.2024.2412431","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Aim:Acinetobacter baumannii (AB) is a clinically important bacterial pathogen responsible for nosocomial infections. The biofilm-forming capability of these pathogens reduces the antibiotic penetration and its efficacy, thereby complicating the treatment. The current work aims to isolate the most potent biofilm-forming Acinetobacter species from clinical isolates of the patient samples and to evaluate the efficacy of the amikacin-humic acid combination against it.Methods: The combination effect of Amikacin-Humic (AMK-HUM) acid against the highest biofilm-producing A. baumannii SLMK001 was studied via in-vitro (microscopic analysis) and in-silico (Network Pharmacology) analysis.Results: The amikacin-humic acid combination significantly inhibited both the biofilm formation and cell viability of A. baumannii SLMK001. The images observed via Scanning Electron Microscope (SEM) showed a significant decrease in the biofilm matrix. Confocal Laser Scanning Microscope (CLSM) confirmed a reduction of the Z value of its three-dimensional structure. Further, the Network Pharmacology approach supported these experimental findings by identifying the key targets of the amikacin-humic acid combination against the biofilm pathways of A. baumannii.Conclusion: The in-vitro results aligned with the in-silico findings, indicating that the AMK-HUM combination is a promising treatment that significantly activates the key proteins against A. baumannii biofilm formation and pathogenesis.
目的:鲍曼不动杆菌(AB)是临床上造成医院内感染的重要细菌病原体。这些病原体的生物膜形成能力降低了抗生素的穿透力和疗效,从而使治疗复杂化。目前的工作旨在从临床分离的患者样本中分离出最有生物膜形成能力的醋氨曲霉菌,并评估阿米卡星-腐植酸联合疗法对其的疗效:方法:通过体外(显微镜分析)和体内(网络药理学)分析,研究了阿米卡星-腐植酸(AMK-HUM)复方制剂对产生生物膜能力最强的鲍曼不动杆菌SLMK001的疗效:结果:阿米卡星-腐植酸组合能显著抑制鲍曼不动杆菌 SLMK001 的生物膜形成和细胞活力。扫描电子显微镜(SEM)观察到的图像显示,生物膜基质明显减少。共焦激光扫描显微镜(CLSM)证实其三维结构的 Z 值有所降低。此外,网络药理学方法通过确定阿米卡星-胡敏酸组合抗鲍曼尼氏菌生物膜途径的关键靶点,支持了这些实验结果:体外实验结果与体内实验结果一致,表明阿米卡星-胡敏酸组合是一种很有前景的治疗方法,它能显著激活关键蛋白,阻止鲍曼不动杆菌生物膜的形成和致病。
期刊介绍:
Future Microbiology delivers essential information in concise, at-a-glance article formats. Key advances in the field are reported and analyzed by international experts, providing an authoritative but accessible forum for this increasingly important and vast area of research.