Salinas Joel H, Gordesli-Duatepe Fatma Pinar, Diaz-Sanchez Angelica, Abu-Lail Nehal I
Department of Biomedical Engineering and Chemical Engineering, University of Texas at San Antonio, San Antonio, TX 78249, USA.
Department of Genetics and Bioengineering, Izmir University of Economics, Izmir 35330, Türkiye.
Antibiotics (Basel). 2025 Aug 9;14(8):816. doi: 10.3390/antibiotics14080816.
BACKGROUND/OBJECTIVES: The Type IV pilus assembly system in is a major determinant of its pathogenicity, playing a role in surface-associated functions via the biogenesis of Type IV pili (T4P). Tazobactam (TAZ) is a well-characterized β-lactamase inhibitor, primarily used in combination with β-lactam antibiotics such as piperacillin (PIP) to counteract bacterial resistance mechanisms. While resistance to β-lactam antibiotics has been well studied, the influence of T4P on its susceptibility to TAZ remains largely unexplored. For this reason, we investigated how multidrug-resistant 5075 (AB5075) responds to TAZ by assessing the roles of , , and in bacterial growth and biofilm formation under direct TAZ exposure, with a focus on phenotypic characterization rather than molecular mechanisms.
Bacterial growth kinetics were quantified by measuring the optical densities of cell suspensions and the colony forming units per volume (CFUs/mL) at different time intervals. Time-kill assays and microtiter dish biofilm formation assays were used to evaluate how effectively TAZ can inhibit growth and biofilm formation, respectively.
Time-kill assays confirmed that 32 µg/mL of TAZ inhibited growth in both wild-type (WT) and mutant strains, with the mutant showing initial resistance before eventual inhibition. Biofilm assays showed that the mutant had the highest biofilm formation at 8 h, surpassing the WT strain. A prolonged 32 µg/mL of TAZ exposure (24-36 h) significantly reduced biofilm production across all strains, with inhibition rates reaching 89% for the WT, 82% for the mutant, 91% for the mutant, and 86% for the mutant.
These findings deepen our understanding of the strain-specific roles of T4P components in growth and biofilm regulation in AB5075, and highlight the potential of TAZ as a therapeutic strategy against biofilm-associated infections.
背景/目的：[具体细菌名称]中的IV型菌毛组装系统是其致病性的主要决定因素，通过IV型菌毛（T4P）的生物合成在表面相关功能中发挥作用。他唑巴坦（TAZ）是一种特征明确的β-内酰胺酶抑制剂，主要与哌拉西林（PIP）等β-内酰胺类抗生素联合使用，以对抗细菌耐药机制。虽然[具体细菌名称]对β-内酰胺类抗生素的耐药性已得到充分研究，但T4P对其对TAZ敏感性的影响在很大程度上仍未得到探索。因此，我们通过评估[相关基因]在直接暴露于TAZ的情况下对细菌生长和生物膜形成的作用，研究了多重耐药的[具体细菌名称] 5075（AB5075）对TAZ的反应，重点是表型特征而非分子机制。
通过在不同时间间隔测量细胞悬液的光密度和每体积的菌落形成单位（CFU/mL）来量化细菌生长动力学。采用时间杀菌试验和微量滴定板生物膜形成试验分别评估TAZ抑制生长和生物膜形成的效果。
时间杀菌试验证实，32 μg/mL的TAZ抑制野生型（WT）和突变株的生长，[具体突变株]突变体在最终被抑制之前表现出初始抗性。生物膜试验表明，[具体突变株]突变体在8小时时生物膜形成最多，超过了WT菌株。延长32 μg/mL的TAZ暴露时间（24 - 36小时）显著降低了所有菌株的生物膜产生，WT菌株的抑制率达到89%，[具体突变株]突变体为82%，[具体突变株]突变体为91%，[具体突变株]突变体为86%。
这些发现加深了我们对T4P成分在AB5075生长和生物膜调节中的菌株特异性作用的理解，并突出了TAZ作为对抗生物膜相关感染的治疗策略的潜力。
