金抗肽SIF4对大肠杆菌基于细胞壁靶点的非细胞质膜损伤抑菌机理

Non-Cytoplasmic Membrane Damage Antimicrobial Mechanism of Metal Antimicrobial Peptide SIF4 Against Escherichia coli Based on Cell Wall Target

摘要:

为阐明金抗肽SIF4对食源性大肠杆菌基于细胞壁靶点的非细胞质膜损伤抑菌机理，研究了SIF₄对细胞壁损伤的影响、与细胞壁脂多糖竞争性结合机理及对细胞壁膜组分影响机理，并运用扫描电镜分析了菌体形貌变化。研究发现，SIF₄对菌体细胞壁有破坏作用，在一定浓度范围内，细胞壁受损与SIF₄处理时间和处理剂量呈正相关，且组间差异显著（P<0.05）； SIF₄可与细胞壁脂多糖（LPS）竞争性结合，结合量为256 mg/L或更大时，表现无抑菌活性；傅立叶变换红外光谱（FT-IR）分析发现，SIF₄对细胞壁多糖信息区、蛋白质与脂肪酸混合信息区影响明显，揭示细胞壁是潜在抑菌效应靶点；扫描电镜（SEM）分析发现，SIF₄可破坏菌体细胞壁膜结构并改变菌体形貌。研究认为，SIF₄可基于细胞壁损伤靶点作用于大肠杆菌并实现高效抑菌活性，研究结果可为阐明基于细胞壁靶点的非细胞质膜损伤抑菌机理和食源性大肠杆菌生物防控提供依据。

Abstract:

To elucidate the non-cytoplasmic membrane damage antimicrobial mechanism of metal antimicrobial peptide SIF₄ against foodborne Escherichia coli(E. coli) based on cell wall target, the effect of SIF₄ on cell wall damage, the competitive binding mechanism of SIF₄ with cell wall lipopolysaccharide (LPS), and the effect of SIF₄ on cell wall membrane components were investigated, and the changes in cell morphology of strain were analyzed using scanning electron microscopy. Results displayed that SIF₄ could destroy the bacterial cell wall. Within a certain concentration range, the damage to the cell wall was positively correlated with the treatment time and treatment dose of SIF₄, and the difference between groups was significant (P<0.05). SIF₄could competitively bind with lipopolysaccharides(LPS), however, no antibacterial activity was observed when the binding amount exceeded 256 mg/L. Fourier transform infrared spectroscopy (FT-IR) analysis revealed that SIF₄ had a significant impact on cell wall polysaccharide information area, as well as the mixed information area of protein and fatty acid, indicating that cell wall was the potential antimicrobial targets. Scanning electron microscope (SEM) analysis showed that SIF₄ could destroy the cell wall membrane structure and alter strain morphology. This study suggests that SIF4 can exert efficient antimicrobial activity against E. coli based on cell wall damage target. Research results could provide supports for elucidating the mechanism of non-cytoplasmic membrane damage based on cell wall targets and biological control of foodborne E. coli.