Laboratório de Bioquímica e Microbiologia Aplicada, ICTA-UFRGS, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9500, Porto Alegre, 91501-970, Brazil.
Chromaleont S.R.L., c/o Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, viale Annunziata, 98168, Polo AnnunziataMessina, Italy.
Cell Mol Life Sci. 2022 Apr 28;79(5):263. doi: 10.1007/s00018-022-04292-4.
With the onset of Listeria monocytogenes resistance to the bacteriocin nisin, the search for alternative antimicrobial treatments is of fundamental importance. In this work, we set out to investigate proteins and lipids involved in the resistance mechanisms of L. monocytogenes against the antimicrobial peptides (AMPs) nisin and fengycin. The effect of sub-lethal concentrations of nisin and lipopeptide fengycin secreted by Bacillus velezensis P34 on L. monocytogenes was investigated by mass spectrometry-based lipidomics and proteomics. Both AMPs caused a differential regulation of biofilm formation, confirming the promotion of cell attachment and biofilm assembling after treatment with nisin, whereas growth inhibition was observed after fengycin treatment. Anteiso branched-chain fatty acids were detected in higher amounts in fengycin-treated samples (46.6%) as compared to nisin-treated and control samples (39.4% and 43.4%, respectively). In addition, a higher relative abundance of 30:0, 31:0 and 32:0 phosphatidylglycerol species was detected in fengycin-treated samples. The lipidomics data suggest the inhibition of biofilm formation by the fengycin treatment, while the proteomics data revealed downregulation of important cell wall proteins involved in the building of biofilms, such as the lipoteichoic acid backbone synthesis (Lmo0927) and the flagella-related (Lmo0718) proteins among others. Together, these results provide new insights into the modification of lipid and protein profiles and biofilm formation in L. monocytogenes upon exposure to antimicrobial peptides.
随着李斯特菌对细菌素乳链菌肽的耐药性的出现，寻找替代抗菌治疗方法变得至关重要。在这项工作中，我们着手研究参与李斯特菌抵抗抗菌肽（AMPs）乳链菌肽和丰原素的耐药机制的蛋白质和脂质。通过基于质谱的脂质组学和蛋白质组学研究了枯草芽孢杆菌 P34 分泌的亚致死浓度的乳链菌肽和脂肽丰原素对李斯特菌的影响。两种 AMPs 都导致生物膜形成的差异调节，证实了乳链菌肽处理后促进细胞附着和生物膜组装，而丰原素处理后则观察到生长抑制。与乳链菌肽处理和对照样品（分别为 39.4%和 43.4%）相比，丰原素处理样品中检测到更高含量的支链 anteiso 脂肪酸（46.6%）。此外，丰原素处理样品中还检测到更高相对丰度的 30:0、31:0 和 32:0 磷脂酰甘油种。脂质组学数据表明丰原素处理抑制生物膜形成，而蛋白质组学数据显示与生物膜形成有关的细胞壁蛋白的下调，如脂磷壁酸骨架合成（Lmo0927）和鞭毛相关（Lmo0718）蛋白等。总之，这些结果提供了新的见解，即暴露于抗菌肽后，李斯特菌的脂质和蛋白质谱以及生物膜形成的修饰。
