2015
DOI: 10.1016/j.bbamem.2015.03.007
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Increased membrane surface positive charge and altered membrane fluidity leads to cationic antimicrobial peptide resistance in Enterococcus faecalis

Abstract: To understand the role of cell membrane phospholipids during resistance development to cationic antimicrobial peptides (CAMPs) in Enterococcus faecalis, gradual dose-dependent single exposure pediocin-resistant (Pedr) mutants of E. faecalis (Efv2.1, Efv3.1, Efv3.2, Efv4.1, Efv4.2, Efv5.1, Efv5.2 and Efv5.3), conferring simultaneous resistance to other CAMPs, selected in previous study were characterized for cell membrane phospholipid head-groups and fatty acid composition. The involvement of phospholipids in r… Show more

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Cited by 90 publications
(72 citation statements)
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“…Remodeling of bacterial surfaces is a hallmark mechanism of resistance to cationic antimicrobial peptides (cAMPs). The remodeling can occur in various parts of the envelope, from the capsule (51) to lipid A remodeling (5), LPS decoration (52), fatty acid composition changes (53), and PG modifications (54,55). Two-component regulatory systems like PhoP/PhoQ and PmrA/PmrB respond to cAMPs in the environment, triggering the expression of genes involved in cell surface remodeling.…”
Section: Discussionmentioning
confidence: 99%
“…Remodeling of bacterial surfaces is a hallmark mechanism of resistance to cationic antimicrobial peptides (cAMPs). The remodeling can occur in various parts of the envelope, from the capsule (51) to lipid A remodeling (5), LPS decoration (52), fatty acid composition changes (53), and PG modifications (54,55). Two-component regulatory systems like PhoP/PhoQ and PmrA/PmrB respond to cAMPs in the environment, triggering the expression of genes involved in cell surface remodeling.…”
Section: Discussionmentioning
confidence: 99%
“…The effects of aa-PG on antibiotic resistance have been investigated in several important human pathogens such as S. aureus (for review see [4]), L. monocytogenes , 53 B. anthracis , 58 P. aeruginosa , 24,59 M. tuberculosis , 29,60 Enterococcus species, 35,36,61 and B. subtilis 62,63 (for review see [1]). aa-PGs in these organisms primarily enhance bacterial resistance to positively charged compounds targeting the membrane (such as CAMPs) and last resort lipopetides like daptomycin.…”
Section: Increased Virulence and Antibiotic Resistance Linked To Lipimentioning
confidence: 99%
“…As PagP is involved in the homeostasis of membrane hydrophobicity, it is certainly imaginable that the protein may also repair AMP-damaged membranes, which would constitute another AMP resistance mechanism [134]. In general, higher membrane rigidity can be achieved by an increase of saturated acyl chains in the membrane, which has been reported to confer elevated resistance to pediocin and nisin in E. faecalis and L. monocytogenes, respectively [135,136]. In S. aureus, enhanced membrane rigidity can be achieved by increased incorporation of the carotenoid staphyloxanthin, which stabilizes acyl chains in the membrane [137].…”
Section: Alteration Of the Cytoplasmic Membrane Structurementioning
confidence: 99%