Resistance to Antimicrobial Peptides in Vibrios

Type Article
Date 2014-12
Language English
Author(s) Destoumieux-Garzón Delphine1, Duperthuy Marylise2, Vanhove Audrey1, Schmitt Paulina3, Wai Sun2
Affiliation(s) 1 : Ecology of Coastal Marine Systems, CNRS, Ifremer, University of Montpellier, IRD, Place Eugène Bataillon, CC80, 34095 Montpellier, France
2 : Department of Molecular Biology, The Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, 901 87 Umeå, Sweden;
3 : Laboratorio de Genética e Inmunología Molecular, Instituto de Biología, Pontificia Universidad Católica de Valparaíso, Avenida Universidad 330, 2373223 Valparaíso, Chile
Source Antibiotics (2079-6382) (MDPI AG), 2014-12 , Vol. 3 , N. 4 , P. 540-563
DOI 10.3390/antibiotics3040540
Note This article belongs to the Special Issue Antimicrobial Peptides
Keyword(s) vibrio, lipopolysaccharide, outer membrane vesicle, membrane transporter, innate immunity, defensin, cathelicidin, bactericidal/permeability-increasing protein
Abstract Vibrios are associated with a broad diversity of hosts that produce antimicrobial peptides (AMPs) as part of their defense against microbial infections. In particular, vibrios colonize epithelia, which function as protective barriers and express AMPs as a first line of chemical defense against pathogens. Recent studies have shown they can also colonize phagocytes, key components of the animal immune system. Phagocytes infiltrate infected tissues and use AMPs to kill the phagocytosed microorganisms intracellularly, or deliver their antimicrobial content extracellularly to circumvent tissue infection. We review here the mechanisms by which vibrios have evolved the capacity to evade or resist the potent antimicrobial defenses of the immune cells or tissues they colonize. Among their strategies to resist killing by AMPs, primarily vibrios use membrane remodeling mechanisms. In particular, some highly resistant strains substitute hexaacylated Lipid A with a diglycine residue to reduce their negative surface charge, thereby lowering their electrostatic interactions with cationic AMPs. As a response to envelope stress, which can be induced by membrane-active agents including AMPs, vibrios also release outer membrane vesicles to create a protective membranous shield that traps extracellular AMPs and prevents interaction of the peptides with their own membranes. Finally, once AMPs have breached the bacterial membrane barriers, vibrios use RND efflux pumps, similar to those of other species, to transport AMPs out of their cytoplasmic space.
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