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@ARTICLE{Krall:178324,
      author       = {L. J. Krall and S. Klein and S. Boutin and C. C. Wu and A.
                      Sähr and M. L. Stanifer and S. Boulant$^*$ and K. Heeg and
                      D. Nurjadi and D. Hildebrand},
      title        = {{I}nvasiveness of {E}scherichia coli {I}s {A}ssociated with
                      an {I}nc{FII} {P}lasmid.},
      journal      = {Pathogens},
      volume       = {10},
      number       = {12},
      issn         = {2076-0817},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2021-03271},
      pages        = {1645},
      year         = {2021},
      abstract     = {Escherichia coli is one of the most prevalent pathogens,
                      causing a variety of infections including bloodstream
                      infections. At the same time, it can be found as a
                      commensal, being part of the intestinal microflora. While it
                      is widely accepted that pathogenic strains can evolve from
                      colonizing E. coli strains, the evolutionary route
                      facilitating the commensal-to-pathogen transition is complex
                      and remains not fully understood. Identification of the
                      underlying mechanisms and genetic changes remains
                      challenging. To investigate the factors involved in the
                      transition from intestinal commensal to invasive E. coli
                      causing bloodstream infections, we compared E. coli isolated
                      from blood culture to isolates from the rectal flora of the
                      same individuals by whole genome sequencing to identify
                      clonally related strains and potentially relevant virulence
                      factors. in vitro invasion assays using a Caco- 2 cell
                      intestinal epithelial barrier model and a gut organoid model
                      were performed to compare clonally related E. coli. The
                      experiments revealed a correlation between the presence of
                      an IncFII plasmid carrying hha and the degree of
                      invasiveness. In summary, we provide evidence for the role
                      of an IncFII plasmid in the transition of colonization to
                      invasion in clinical E. coli isolates.},
      keywords     = {Escherichia coli (Other) / IncFII plasmid (Other) /
                      bloodstream infection (Other) / gut organoid model (Other) /
                      hha (Other) / invasion (Other)},
      cin          = {F140},
      ddc          = {610},
      cid          = {I:(DE-He78)F140-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34959600},
      doi          = {10.3390/pathogens10121645},
      url          = {https://inrepo02.dkfz.de/record/178324},
}