Salmonella is a genus of widely spread Gram negative, facultative anaerobic bacteria, which is known to cause ¼th of diarrheal morbidity and mortality globally. It causes typhoid fever and gastroenteritis by gaining access to the host gut through contaminated food and water. Salmonella utilizes its biofilm lifestyle to strongly resist antibiotics and persist in the host. Although biofilm removal or dispersal has been studied widely, the inhibition of the initiation of Salmonella biofilm remains elusive. This study was conducted to determine the anti-biofilm property of the cell-free supernatant obtained from a carbon-starvation inducible proline peptide transporter mutant (ΔyjiY) strain. Our study shows that Salmonella ΔyjiY culture supernatant primarily inhibits biofilm initiation by regulating biofilm-associated transcriptional network. This work demonstrates that highly abundant proteases such as HslV and GrpE cleave the protein aggregates, whereas global transcription regulators H-NS, FlgM regulate expression of SPIs and flagellar genes. Relatively low abundances of flavoredoxin, glutaredoxin, thiol peroxidase etc. leads to accumulation of ROS within the biofilm, and subsequent toxicity. This work further suggests that targeting these oxidative stress relieving proteins might be a good druggable choice to reduce Salmonella biofilm.

中文翻译：

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鼠伤寒沙门氏菌肽转运蛋白突变体无细胞上清液的全球转录调控导致物种内生物膜启动的抑制。

沙门氏菌是广泛传播的革兰氏阴性兼性厌氧细菌的一种，已知这种细菌会导致全球腹泻发病率和死亡率的四分之一。它通过被污染的食物和水进入宿主肠道而引起伤寒和肠胃炎。沙门氏菌利用其生物膜生活方式强烈抵抗抗生素并在宿主中持久存在。尽管已经广泛地研究了生物膜的去除或分散，但是抑制沙门氏菌生物膜的启动仍然难以捉摸。进行该研究以确定从碳饥饿诱导的脯氨酸肽转运蛋白突变体（ΔyjiY）菌株获得的无细胞上清液的抗生物膜特性。我们的研究表明沙门氏菌ΔyjiY培养物上清液主要通过调节生物膜相关的转录网络来抑制生物膜的启动。这项工作表明，高度丰富的蛋白酶（例如HslV和GrpE）可裂解蛋白质聚集体，而全局转录调节剂H-NS，FlgM则可调节SPI和鞭毛基因的表达。调味品毒素，戊二醛毒素，硫醇过氧化物酶等的相对较低的丰度会导致ROS在生物膜内积聚，并随之产生毒性。这项工作进一步表明，靶向这些氧化应激缓解蛋白可能是减少沙门氏菌生物膜的良好药物选择。