Bacteria are increasingly relying on biofilms to develop resistance to antibiotics thereby resulting in their failure in treating many infections. In spite of continuous research on many synthetic and natural compounds, ideal anti-biofilm molecule is still not found thereby warranting search for new class of molecules. The current study focuses on exploring anti-biofilm potential of selenocystine against respiratory tract infection (RTI)-causing bacteria. Anti-bacterial and anti-biofilm assays demonstrated that selenocystine inhibits the growth of bacteria in their planktonic state, and formation of biofilms while eradicating preformed-biofilm effectively. Selenocystine at a MIC 50 as low as 42 and 28 μg/mL effectively inhibited the growth of Klebsiella pneumonia and Pseudomonas aeruginosa . The antibacterial effect is further reconfirmed by agar cup diffusion assay and growth-kill assay. Selenocystine showed 30–60% inhibition of biofilm formation in K. pneumonia, and 44–70% in P. aeruginosa respectively. It also distorted the preformed-biofilms by degrading the eDNA component of the Extracellular Polymeric Substance matrix. Molecular docking studies of selenocystine with quorum sensing specific proteins clearly showed that through the carboxylic acid moiety it interacts and inhibits the protein function, thereby confirming its anti-biofilm potential. With further validation selenocystine can be explored as a potential candidate for the treatment of RTIs.

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阐明硒代胱氨酸对引起细菌的呼吸道感染的抗生物膜和抗群体感应潜力：体外和计算机研究

细菌越来越依赖生物膜来产生对抗生素的抗性，从而导致它们无法治疗许多感染。尽管对许多合成和天然化合物进行了不断的研究，但仍未找到理想的抗生物膜分子，因此需要寻找新的分子类别。目前的研究重点是探索硒代半胱氨酸对引起呼吸道感染 (RTI) 的细菌的抗生物膜潜力。抗菌和抗生物膜试验表明，硒代半胱氨酸抑制浮游状态下细菌的生长和生物膜的形成，同时有效地根除预先形成的生物膜。MIC 50 低至 42 和 28 μg/mL 的硒代胱氨酸有效抑制肺炎克雷伯菌和铜绿假单胞菌的生长。琼脂杯扩散试验和生长杀伤试验进一步证实了抗菌作用。Selenocystine 在肺炎克雷伯菌中显示出 30-60% 的生物膜形成抑制作用，在铜绿假单胞菌中显示出 44-70% 的抑制作用。它还通过降解细胞外聚合物基质的 eDNA 成分来扭曲预先形成的生物膜。硒代胱氨酸与群体感应特定蛋白质的分子对接研究清楚地表明，它通过羧酸部分相互作用并抑制蛋白质功能，从而证实了其抗生物膜的潜力。随着进一步的验证，硒代胱氨酸可以作为治疗 RTI 的潜在候选药物进行探索。它还通过降解细胞外聚合物基质的 eDNA 成分来扭曲预先形成的生物膜。硒代胱氨酸与群体感应特定蛋白质的分子对接研究清楚地表明，它通过羧酸部分相互作用并抑制蛋白质功能，从而证实了其抗生物膜的潜力。随着进一步的验证，硒代胱氨酸可以作为治疗 RTI 的潜在候选药物进行探索。它还通过降解细胞外聚合物基质的 eDNA 成分来扭曲预先形成的生物膜。硒代胱氨酸与群体感应特定蛋白质的分子对接研究清楚地表明，它通过羧酸部分相互作用并抑制蛋白质功能，从而证实了其抗生物膜的潜力。随着进一步的验证，硒代胱氨酸可以作为治疗 RTI 的潜在候选药物进行探索。