Gene expression profiling of Burkholderia cenocepacia at the time of cepacia syndrome: loss of motility as a marker of poor prognosis?
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
25694518
PubMed Central
PMC4400763
DOI
10.1128/jcm.03605-14
PII: JCM.03605-14
Knihovny.cz E-zdroje
- MeSH
- bakteriemie mikrobiologie MeSH
- biogeneze organel * MeSH
- Burkholderia cenocepacia genetika fyziologie MeSH
- cystická fibróza komplikace mikrobiologie MeSH
- dospělí MeSH
- flagella genetika fyziologie MeSH
- infekce bakteriemi rodu Burkholderia mikrobiologie MeSH
- krev mikrobiologie MeSH
- lidé MeSH
- lokomoce MeSH
- mikročipová analýza MeSH
- prognóza MeSH
- retrospektivní studie MeSH
- sputum mikrobiologie MeSH
- stanovení celkové genové exprese * MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
Cepacia syndrome (CS) is a fatal septic condition that develops in approximately 20% of cystic fibrosis (CF) patients chronically infected with the Burkholderia cepacia complex (Bcc). The most common causative agent is Burkholderia cenocepacia, a clinically dominant Bcc species that contains the globally distributed epidemic strain sequence type 32 (ST32). Using microarrays, we compared the transcriptomes of ST32 isolates from the bloodstream at the time of CS with their sputum counterparts recovered 1 to 2 months prior to the development of CS. Global gene expression profiles of blood isolates revealed greater activities of the virulence genes involved in the type III secretion system, the bacterial exopolysaccharide cepacian, and quorum sensing, while reduced expression was demonstrated for flagellar genes. Furthermore, a nonmotile phenotype (as evaluated by a swimming motility assay) was identified in blood isolates from 6 out of 8 patients with CS; this phenotype was traceable to 24 months prior to the onset of CS. Loss of motility was not observed in any of the 89 ST32 isolates recovered over the course of chronic infection from 17 patients without CS. In conclusion, the gene expression of Bcc bacteria disseminated during CS has been elucidated for the first time. This study demonstrated marked differences at the transcriptome level between isogenic ST32 isolates that are attributable to the stage and site of infection. The finding of a nonmotile B. cenocepacia isolate may serve as a warning sign for the development of CS in the near future.
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