Biswal Sarmistha, Caetano Karina, Jain Diamond, Sarrila Anusha, Munshi Tulika, Dickman Rachael, Tabor Alethea B, Rath Surya Narayan, Bhakta Sanjib, Ghosh Anindya S
Molecular Microbiology Laboratory, Department of Biotechnology, Indian Institute of Technology Kharagpur, Kharagpur 721302, West Bengal, India.
Mycobacteria Research Laboratory, Institute of Structural and Molecular Biology, Department of Biological Sciences, Birkbeck, University of London, Malet Street, London WC1E 7HX, UK.
Antibiotics (Basel). 2023 Mar 10;12(3):553. doi: 10.3390/antibiotics12030553.
Class A serine β-lactamases (SBLs) have a conserved non-active site structural domain called the omega loop (Ω-loop), in which a glutamic acid residue is believed to be directly involved in the hydrolysis of β-lactam antibiotics by providing a water molecule during catalysis. We aimed to design and characterise potential pentapeptides to mask the function of the Ω-loop of β-lactamases and reduce their efficacy, along with potentiating the β-lactam antibiotics and eventually decreasing β-lactam resistance. Considering the Ω-loop sequence as a template, a group of pentapeptide models were designed, validated through docking, and synthesised using solid-phase peptide synthesis (SPPS). To check whether the β-lactamases (BLAs) were inhibited, we expressed specific BLAs (TEM-1 and SHV-14) and evaluated the trans-expression through a broth dilution method and an agar dilution method (HT-SPOTi). To further support our claim, we conducted a kinetic analysis of BLAs with the peptides and employed molecular dynamics (MD) simulations of peptides. The individual presence of six histidine-based peptides (TSHLH, ETHIH, ESRLH, ESHIH, ESRIH, and TYHLH) reduced β-lactam resistance in the strains harbouring BLAs. Subsequently, we found that the combinational effect of these peptides and β-lactams sensitised the bacteria towards the β-lactam drugs. We hypothesize that the antimicrobial peptides obtained might be considered among the novel inhibitors that can be used specifically against the Ω-loop of the β-lactamases.
A类丝氨酸β-内酰胺酶(SBLs)有一个保守的非活性位点结构域,称为ω环(Ω环),其中一个谷氨酸残基被认为通过在催化过程中提供一个水分子直接参与β-内酰胺抗生素的水解。我们旨在设计并表征潜在的五肽,以掩盖β-内酰胺酶Ω环的功能并降低其效力,同时增强β-内酰胺抗生素的作用并最终降低β-内酰胺耐药性。以Ω环序列为模板,设计了一组五肽模型,通过对接进行验证,并使用固相肽合成(SPPS)进行合成。为了检查β-内酰胺酶(BLAs)是否受到抑制,我们表达了特定的BLAs(TEM-1和SHV-14),并通过肉汤稀释法和琼脂稀释法(HT-SPOTi)评估了转表达。为了进一步支持我们的观点,我们对BLAs与这些肽进行了动力学分析,并对肽进行了分子动力学(MD)模拟。六种基于组氨酸的肽(TSHLH、ETHIH、ESRLH、ESHIH、ESRIH和TYHLH)单独存在时降低了携带BLAs的菌株中的β-内酰胺耐药性。随后,我们发现这些肽与β-内酰胺的联合作用使细菌对β-内酰胺类药物敏感。我们假设所获得的抗菌肽可能被视为可专门用于对抗β-内酰胺酶Ω环的新型抑制剂。