Salazar Maria, Shahbazi Nia Siavash, German Nadezhda A, Awosile Babafela, Sabiu Saheed, Calle Alexandra
School of Veterinary Medicine, Texas Tech University, Amarillo, TX, United States.
School of Pharmacy, Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX, United States.
Front Microbiol. 2024 Sep 25;15:1399996. doi: 10.3389/fmicb.2024.1399996. eCollection 2024.
is a bacterial pathogen of considerable significance in public health, capable of inducing a diverse range of infectious diseases. One of the most notorious mechanisms used by to survive and colonize the site of infection is its ability to form biofilms. Diflunisal, a non-steroidal anti-inflammatory drug (NSAID), is a known inhibitor of the Agr system in , which is key in regulating biofilm formation. This study evaluated the effect of broad-spectrum antibiotics in combination with diflunisal on biofilm density. Eight antibiotics were tested independently at different concentrations and in combination with diflunisal to assess their effect on biofilm formation. When using the antibiotics alone and with diflunisal, a significant control effect on biofilm formation was observed ( < 0.05), irrespective of diflunisal presence, but did not achieve a complete biofilm growth inhibition. Over time, diflunisal influenced biofilm formation; however, such an effect was correlated with antibiotic concentration and exposure time. With amikacin treatments, biofilm density increased with extended exposure time. In the case of imipenem, doripenem, levofloxacin, and ciprofloxacin, lower doses and absence of diflunisal showed higher control over biofilm growth with longer exposure. However, in all cases, diflunisal did not significantly affect the treatment effect on biofilm formation. In the absence of antibiotics, diflunisal significantly reduced biofilm formation by 53.12% ( < 0.05). This study suggests that diflunisal could be a potential treatment to control biofilms, but it does not enhance biofilm inhibition when combined with antibiotics.
是一种在公共卫生领域具有相当重要意义的细菌病原体，能够引发多种传染病。它用于在感染部位存活和定殖的最臭名昭著的机制之一是其形成生物膜的能力。双氟尼酸是一种非甾体抗炎药（NSAID），是已知的抑制其Agr系统的物质，而Agr系统在调节生物膜形成中起关键作用。本研究评估了广谱抗生素与双氟尼酸联合使用对生物膜密度的影响。对八种抗生素在不同浓度下单独以及与双氟尼酸联合进行测试，以评估它们对生物膜形成的影响。单独使用抗生素以及与双氟尼酸联合使用时，无论双氟尼酸是否存在，均观察到对生物膜形成有显著的控制作用（<0.05），但未实现生物膜生长的完全抑制。随着时间推移，双氟尼酸影响生物膜形成；然而，这种影响与抗生素浓度和暴露时间相关。使用阿米卡星治疗时，生物膜密度随暴露时间延长而增加。对于亚胺培南、多立培南、左氧氟沙星和环丙沙星，较低剂量且不存在双氟尼酸时，随着暴露时间延长对生物膜生长的控制效果更好。然而，在所有情况下，双氟尼酸对生物膜形成的治疗效果均无显著影响。在不存在抗生素的情况下，双氟尼酸使生物膜形成显著减少53.12%（<0.05）。本研究表明，双氟尼酸可能是控制生物膜的一种潜在治疗方法，但与抗生素联合使用时不会增强生物膜抑制作用。
