肠球菌法定人数控制蛋白酶改变了噬菌体感染。

FEMS microbes Pub Date : 2024-07-26 eCollection Date: 2024-01-01 DOI:10.1093/femsmc/xtae022
Emma K Sheriff, Fernanda Salvato, Shelby E Andersen, Anushila Chatterjee, Manuel Kleiner, Breck A Duerkop
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引用次数: 0

摘要

耐多药细菌感染的日益流行引发了人们对包括噬菌体(噬菌体)在内的替代抗菌药物的兴趣。由于对噬菌体感染过程的了解有限,我们无法充分利用噬菌体的治疗潜力。为了了解噬菌体的感染动态,我们对感染了噬菌体 VPE25 的粪肠球菌进行了蛋白质组学研究。我们发现,在噬菌体感染粪肠球菌的过程中会产生大量未表征的噬菌体蛋白。此外,我们还确定了感染期间细菌蛋白质丰度的数百种变化。其中一种蛋白质是肠球菌明胶酶(GelE),它是一种参与生物膜形成和毒力的 fsr 法定量感应调控蛋白酶。斑块试验表明,法定量感应调节因子fsrA或GelE的突变会导致斑块呈现 "光环 "形态,且直径明显增大,这表明对噬菌体感染的保护能力下降。在噬菌体感染过程中,与 GelE 相关的保护作用依赖于假定的软脂水解酶调节因子 LrgA 和抗高蛋白样蛋白 LrgB,它们的表达已被证明受到 GelE 的调控。我们的研究成果可用于开发噬菌体疗法,调节 GelE 的产生,从而改变生物膜的形成并降低粪肠球菌的毒力。
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Enterococcal quorum-controlled protease alters phage infection.

Increased prevalence of multidrug-resistant bacterial infections has sparked interest in alternative antimicrobials, including bacteriophages (phages). Limited understanding of the phage infection process hampers our ability to utilize phages to their full therapeutic potential. To understand phage infection dynamics, we performed proteomics on Enterococcus faecalis infected with the phage VPE25. We discovered that numerous uncharacterized phage proteins are produced during phage infection of E. faecalis. Additionally, we identified hundreds of changes in bacterial protein abundances during infection. One such protein, enterococcal gelatinase (GelE), an fsr quorum-sensing-regulated protease involved in biofilm formation and virulence, was reduced during VPE25 infection. Plaque assays showed that mutation of either the quorum-sensing regulator fsrA or gelE resulted in plaques with a "halo" morphology and significantly larger diameters, suggesting decreased protection from phage infection. GelE-associated protection during phage infection is dependent on the putative murein hydrolase regulator LrgA and antiholin-like protein LrgB, whose expression have been shown to be regulated by GelE. Our work may be leveraged in the development of phage therapies that can modulate the production of GelE thereby altering biofilm formation and decreasing E. faecalis virulence.

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