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10.1038/srep17359

http://scihub22266oqcxt.onion/10.1038/srep17359
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suck abstract from ncbi


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pmid26612456
      Sci+Rep 2015 ; 5 (ä): 17359
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  • Cultured enterocytes internalise bacteria across their basolateral surface for, pathogen-inhibitable, trafficking to the apical compartment #MMPMID26612456
  • Dean P ; Quitard S ; Bulmer DM ; Roe AJ ; Kenny B
  • Sci Rep 2015[Nov]; 5 (ä): 17359 PMID26612456 show ga
  • In vitro- and in vivo-polarised absorptive epithelia (enterocytes) are considered to be non-phagocytic towards bacteria with invasive pathogenic strains relying on virulence factors to 'force' entry. Here, we report a serendipitous discovery that questions these beliefs. Thus, we uncover in well-established models of human small (Caco-2; TC-7) and large (T84) intestinal enterocytes a polarization-dependent mechanism that can transfer millions of bacteria from the basal to apical compartment. Antibiotic-protection assays, confocal imaging and drug inhibitor data are consistent with a transcellular route in which internalized, basolateral-membrane enclosed bacteria are trafficked to and across the apical surface. Basal-to-apical transport of non-pathogenic bacteria (and inert beads) challenged the idea of pathogens relying on virulence factors to force entry. Indeed, studies with Salmonella demonstrated that it's entry-forcing virulence factor (SPI-I) was not required to enter via the basolateral surface but to promote another virulence-associated event (intra-enterocyte accumulation).
  • |*Bacterial Translocation [MESH]
  • |Biological Transport [MESH]
  • |Caco-2 Cells [MESH]
  • |Cell Line [MESH]
  • |Cell Polarity/physiology [MESH]
  • |Enterocytes/drug effects/*microbiology [MESH]
  • |Enteropathogenic Escherichia coli/pathogenicity/physiology [MESH]
  • |HeLa Cells [MESH]
  • |Humans [MESH]
  • |Salmonella typhimurium/pathogenicity/physiology [MESH]


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