Publication:
Virulence determinants of colistin-resistant K. pneumoniae high-risk clones

dc.contributor.departmentDepartment of Industrial Engineering
dc.contributor.departmentGraduate School of Health Sciences
dc.contributor.departmentSchool of Medicine
dc.contributor.kuauthorAlbayrak, Özgür
dc.contributor.kuauthorAtaç, Nazlı
dc.contributor.kuauthorCan, Füsun
dc.contributor.kuauthorDemiray, Atalay
dc.contributor.kuauthorDoğan, Özlem
dc.contributor.kuauthorGönen, Mehmet
dc.contributor.kuauthorKarahüseyinoğlu, Serçin
dc.contributor.kuauthorKılıçoğlu, Bilge Kaan
dc.contributor.kuauthorŞahin, Özgün Ekin
dc.contributor.kuauthorVatansever, Cansel
dc.contributor.kuauthorErgönül, Önder
dc.contributor.schoolcollegeinstituteCollege of Engineering
dc.contributor.schoolcollegeinstituteGRADUATE SCHOOL OF HEALTH SCIENCES
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2024-11-09T13:52:23Z
dc.date.issued2021
dc.description.abstractWe proposed the hypothesis that high-risk clones of colistin-resistant K. pneumoniae (ColR-Kp) possesses a high number of virulence factors and has enhanced survival capacity against the neutrophil activity. We studied virulence genes of ColR-Kp isolates and neutrophil response in 142 patients with invasive ColR-Kp infections. The ST101 and ST395 ColR-Kp infections had higher 30-day mortality (58%, p = 0.005 and 75%, p = 0.003). The presence of yersiniabactin biosynthesis gene (ybtS) and ferric uptake operon associated gene (kfu) were significantly higher in ST101 (99%, p <= 0.001) and ST395 (94%, p < 0.012). Being in ICU (OR: 7.9; CI: 1.43-55.98; p = 0.024), kfu (OR:27.0; CI: 5.67-179.65; p < 0.001) and ST101 (OR: 17.2; CI: 2.45-350.40; p = 0.01) were found to be predictors of 30-day mortality. Even the neutrophil uptake of kfu+-ybtS+ ColR-Kp was significantly higher than kfu--ybtS- ColR-Kp (phagocytosis rate: 78% vs. 65%, p < 0.001), and the kfu+-ybtS+ ColR-Kp survived more than kfu--ybtS- ColR-Kp (median survival index: 7.90 vs. 4.22; p = 0.001). The kfu+-ybtS+ ColR-Kp stimulated excessive NET formation. Iron uptake systems in high-risk clones of colistin-resistant K. pneumoniae enhance the success of survival against the neutrophil phagocytic defense and stimulate excessive NET formation. The drugs targeted to iron uptake systems would be a promising approach for the treatment of colistin-resistant high-risk clones of K. pneumoniae infections.
dc.description.fulltextYES
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue5
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipTurkish Academy of Sciences (TUBA) Young Scientist Award Program
dc.description.sponsorshipScience Academy of Turkey (BAGEP) The Young Scientist Award Program
dc.description.versionPublisher version
dc.description.volume10
dc.identifier.doi10.3390/biology10050436
dc.identifier.eissn2079-7737
dc.identifier.embargoNO
dc.identifier.filenameinventorynoIR03026
dc.identifier.quartileQ2
dc.identifier.scopus2-s2.0-85106590248
dc.identifier.urihttps://hdl.handle.net/20.500.14288/3981
dc.identifier.wos653479500001
dc.keywordsColistin resistance
dc.keywordsPneumoniae
dc.keywordsIron uptake
dc.keywordsNet formation
dc.keywordsPhagocytosis
dc.language.isoeng
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI)
dc.relation.grantnoNA
dc.relation.ispartofBiology
dc.relation.urihttp://cdm21054.contentdm.oclc.org/cdm/ref/collection/IR/id/9682
dc.subjectBiology
dc.subjectLife sciences
dc.subjectBiomedicine
dc.titleVirulence determinants of colistin-resistant K. pneumoniae high-risk clones
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorErgönül, Mehmet Önder
local.contributor.kuauthorGönen, Mehmet
local.contributor.kuauthorCan, Füsun
local.contributor.kuauthorDoğan, Özlem
local.contributor.kuauthorVatansever, Cansel
local.contributor.kuauthorAtaç, Nazlı
local.contributor.kuauthorAlbayrak, Özgür
local.contributor.kuauthorKarahüseyinoğlu, Serçin
local.contributor.kuauthorŞahin, Özgün Ekin
local.contributor.kuauthorKılıçoğlu, Bilge Kaan
local.contributor.kuauthorDemiray, Atalay
local.publication.orgunit1SCHOOL OF MEDICINE
local.publication.orgunit1GRADUATE SCHOOL OF HEALTH SCIENCES
local.publication.orgunit1College of Engineering
local.publication.orgunit2Department of Industrial Engineering
local.publication.orgunit2School of Medicine
local.publication.orgunit2Graduate School of Health Sciences
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