Outer Membrane Vesiculation Facilitates Surface Exchange and In Vivo Adaptation of Vibrio cholerae.
Autor: | Zingl FG; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria., Kohl P; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria., Cakar F; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria., Leitner DR; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria., Mitterer F; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria., Bonnington KE; Duke University Medical Center, Durham, NC 27710, USA., Rechberger GN; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria; Center for Explorative Lipidomics, BioTechMed Graz, 8010 Graz, Austria., Kuehn MJ; Duke University Medical Center, Durham, NC 27710, USA., Guan Z; Department of Biochemistry, Duke University Medical Center, Durham, NC 27710, USA., Reidl J; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria; BioTechMed Graz, 8010 Graz, Austria., Schild S; Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria; BioTechMed Graz, 8010 Graz, Austria. Electronic address: stefan.schild@uni-graz.at. |
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Jazyk: | angličtina |
Zdroj: | Cell host & microbe [Cell Host Microbe] 2020 Feb 12; Vol. 27 (2), pp. 225-237.e8. Date of Electronic Publication: 2019 Dec 31. |
DOI: | 10.1016/j.chom.2019.12.002 |
Abstrakt: | Gram-negative bacteria release outer membrane vesicles into the external milieu to deliver effector molecules that alter the host and facilitate virulence. Vesicle formation is driven by phospholipid accumulation in the outer membrane and regulated by the phospholipid transporter VacJ/Yrb. We use the facultative human pathogen Vibrio cholerae to show that VacJ/Yrb is silenced early during mammalian infection, which stimulates vesiculation that expedites bacterial surface exchange and adaptation to the host environment. Hypervesiculating strains rapidly alter their bacterial membrane composition and exhibit enhanced intestinal colonization fitness. This adaptation is exemplified by faster accumulation of glycine-modified lipopolysaccharide (LPS) and depletion of outer membrane porin OmpT, which confers resistance to host-derived antimicrobial peptides and bile, respectively. The competitive advantage of hypervesiculation is lost upon pre-adaptation to bile and antimicrobial peptides, indicating the importance of these adaptive processes. Thus, bacteria use outer membrane vesiculation to exchange cell surface components, thereby increasing survival during mammalian infection. Competing Interests: Declaration of Interests The authors declare no competing interests. (Copyright © 2019 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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