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Gradual pediocin PA-1 resistance in Enterococcus faecalis confers cross-protection to diverse pore-forming cationic antimicrobial peptides displaying changes in cell wall and mannose PTS expression
- 作者:Rashmi Kumariya ; Shiv Kumar Sood ; Yudhishthir Singh Rajput…
- 关键词:Enterococcus faecalis ; pediocin PA ; 1 ; cationic antimicrobial peptides ; resistance ; permeability barrier
- 刊名:Annals of Microbiology
- 出版年:2015
- 出版时间:June 2015
- 年:2015
- 卷:65
- 期:2
- 页码:721-732
- 全文大小:1,486 KB
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- 作者单位:Rashmi Kumariya (1)
Shiv Kumar Sood (1) Yudhishthir Singh Rajput (1) Anita Kumari Garsa (1)
1. Division of Animal Biochemistry, National Dairy Research Institute, Karnal, Haryana, 132001, India
- 刊物主题:Microbiology; Microbial Genetics and Genomics; Microbial Ecology; Fungus Genetics; Medical Microbiology; Applied Microbiology;
- 出版者:Springer Berlin Heidelberg
- ISSN:1869-2044
文摘
Due to innate and acquired resistance in Enterococcus faecalis against most antibiotics, identification of new alternatives has increased interest in diverse populations of potent cationic antimicrobial peptides (CAMPs) for treatment and natural food biopreservation. The CAMPs, after crossing the cell wall to the periplasmic space, kill their target strain by forming pores in the cell membrane. However, reports of resistance against these CAMPs necessitated the understanding of step(s) interfered with while acquiring this resistance, for designing effective CAMP analogs. In this direction, we selected stable and gradual dose-dependent pediocin PA-1 single exposure resistant (Pedr) mutants of E. faecalis, which conferred cross-protection to diverse CAMPs, viz., HNP-1, nisin and alamethicin but not to polymyxin B, lysozyme and vancomycin. With these Pedr mutants of E. faecalis there was: a gradual neutralization in cell wall surface charge involving D-alanylation of wall teichoic acids (WTA) and lipoteichoic acids (LTA), increase in cell-surface hydrophobicity, increased cell aggregation and biofilm formation and ultra-structural changes in the cell wall, and a reduction of periplasmic space. In addition, a gradual decrease in expression of mannose PTS two (mpt) operon was also observed with distinct changes in growth rate achieving the same biomass production during the stationary phase. These results show that resistance to these CAMPs is not due to mpt directly acting as a docking molecule but due to changes in the cell wall, which increased the permeability barrier to CAMPs diffusion to reach the periplasmic space.
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