Publication:
Phenotypic changes associated with Colistin resistance due to Lipopolysaccharide loss in Acinetobacter baumannii.

dc.contributor.authorCarretero-Ledesma, Marta
dc.contributor.authorGarcia-Quintanilla, Meritxell
dc.contributor.authorMartin-Peña, Reyes
dc.contributor.authorPulido, Marina R
dc.contributor.authorPachon, Jeronimo
dc.contributor.authorMcConnell, Michael J
dc.contributor.funderConsejería de Economía, Ciencia y Empresa of the Junta de Andalucía
dc.contributor.funderSubprograma Miguel Servet from the Ministerio de Economía y Competitividad of Spain
dc.contributor.funderSubprograma Sara Borrell
dc.contributor.funderSpanish Network for the Research in Infectious Diseases
dc.date.accessioned2023-01-25T10:06:25Z
dc.date.available2023-01-25T10:06:25Z
dc.date.issued2018
dc.description.abstractAcinetobacter baumannii can acquire resistance to colistin via complete loss of lipopolysaccharide (LPS) biosynthesis due to mutations in the lpxA, lpxC and lpxD genes. However, although colistin is increasingly being used for the treatment of multidrug resistant infections, very few A. baumannii clinical isolates develop colistin resistance through loss of LPS biosynthesis. This may suggest that LPS loss affects virulence traits that play a role in the transmission and pathogenesis of A. baumannii. In this study we characterize multiple virulence phenotypes of colistin resistant, LPS-deficient derivatives of the ATCC 19606 strain and five multidrug resistant clinical isolates and their colistin resistant, LPS-deficient derivatives. Our results indicate that LPS loss results in growth defects compared to the parental strain in vitro both in laboratory media and human serum (competition indices of 0.58 and 7.0 × 10-7, respectively) and reduced ability to grow and disseminate in vivo (competition index 6.7 × 10-8). Infection with the LPS-deficient strain resulted in lower serum levels of pro-inflammatory cytokines TNF-α and IL-6 compared to the parent strain, and was less virulent in a mouse model of disseminated sepsis. LPS loss also significantly affected biofilm production, surface motility, growth under iron limitation and susceptibility to multiple disinfectants used in the clinical setting. These results demonstrate that LPS loss has a significant effect on multiple virulence traits, and may provide insight into the low incidence of colistin resistant strains lacking LPS that have been reported in the clinical setting.
dc.description.versionSi
dc.identifier.citationCarretero-Ledesma M, García-Quintanilla M, Martín-Peña R, Pulido MR, Pachón J, McConnell MJ. Phenotypic changes associated with Colistin resistance due to Lipopolysaccharide loss in Acinetobacter baumannii. Virulence. 2018 Dec 31;9(1):930-942.
dc.identifier.doi10.1080/21505594.2018.1460187
dc.identifier.essn2150-5608
dc.identifier.pmcPMC5955468
dc.identifier.pmid29638177
dc.identifier.pubmedURLhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5955468/pdf
dc.identifier.unpaywallURLhttps://www.tandfonline.com/doi/pdf/10.1080/21505594.2018.1460187?needAccess=true
dc.identifier.urihttp://hdl.handle.net/10668/12332
dc.issue.number1
dc.journal.titleVirulence
dc.journal.titleabbreviationVirulence
dc.language.isoen
dc.organizationInstituto de Biomedicina de Sevilla-IBIS
dc.organizationHospital Universitario Virgen del Rocío
dc.page.number930-942
dc.provenanceRealizada la curación de contenido 26/06/2025.
dc.publisherLandes Bioscience
dc.pubmedtypeJournal Article
dc.pubmedtypeResearch Support, Non-U.S. Gov't
dc.relation.projectIDCTS 2027
dc.relation.projectIDCPII16/00061
dc.relation.projectIDCD14/00014
dc.relation.projectIDREIPI RD06/0008/0000
dc.relation.publisherversionhttps://www.tandfonline.com/doi/abs/10.1080/21505594.2018.1460187?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
dc.rightsAttribution 4.0 International
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAcinetobacter baumannii
dc.subjectcolistin
dc.subjectfitness
dc.subjectlipopolysaccharide
dc.subjectvirulence
dc.subject.decsColistina
dc.subject.decsLipopolisacáridos
dc.subject.decsBiopelículas
dc.subject.decsDesinfectantes
dc.subject.decsSepsis
dc.subject.decsFenotipo
dc.subject.decsSepsis
dc.subject.meshAcinetobacter Infections
dc.subject.meshAcinetobacter baumannii
dc.subject.meshAnimals
dc.subject.meshAnti-Bacterial Agents
dc.subject.meshBacterial Proteins
dc.subject.meshColistin
dc.subject.meshDrug Resistance, Bacterial
dc.subject.meshFemale
dc.subject.meshHumans
dc.subject.meshInterleukin-6
dc.subject.meshLipopolysaccharides
dc.subject.meshMice, Inbred C57BL
dc.subject.meshMicrobial Sensitivity Tests
dc.subject.meshPhenotype
dc.subject.meshTumor Necrosis Factor-alpha
dc.subject.meshVirulence
dc.titlePhenotypic changes associated with Colistin resistance due to Lipopolysaccharide loss in Acinetobacter baumannii.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number9
dspace.entity.typePublication

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