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  • center
  • program_project
  • nrc
  • whocc
  • project
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  • tool
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  • Assistant Professor
  • Associate Professor
  • Clinical Research Assistant
  • Clinical Research Nurse
  • Clinician Researcher
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  • Lab assistant
  • Master Student
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  • Permanent Researcher
  • Pharmacist
  • PhD Student
  • Physician
  • Post-doc
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  • Research Engineer
  • Retired scientist
  • Technician
  • Undergraduate Student
  • Veterinary
  • Visiting Scientist
  • Deputy Director of Center
  • Deputy Director of Department
  • Deputy Director of National Reference Center
  • Deputy Head of Facility
  • Director of Center
  • Director of Department
  • Director of Institute
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© Research
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Published in Cellular microbiology - 01 Dec 2015

Santos JC, Duchateau M, Fredlund J, Weiner A, Mallet A, Schmitt C, Matondo M, Hourdel V, Chamot-Rooke J, Enninga J

Link to Pubmed [PMID] – 26084942

Link to DOI – 10.1111/cmi.12475

Cell Microbiol 2015 Dec; 17(12): 1699-720

Salmonella invades epithelial cells and survives within a membrane-bound compartment, the Salmonella-containing vacuole (SCV). We isolated and determined the host protein composition of the SCV at 30 min and 3 h of infection to identify and characterize novel regulators of intracellular bacterial localization and growth. Quantitation of the SCV protein content revealed 392 host proteins specifically enriched at SCVs, out of which 173 associated exclusively with early SCVs, 124 with maturing SCV and 95 proteins during both time-points. Vacuole interactions with endoplasmic reticulum-derived coat protein complex II vesicles modulate early steps of SCV maturation, promoting SCV rupture and bacterial hyper-replication within the host cytosol. On the other hand, SCV interactions with VAMP7-positive lysosome-like vesicles promote Salmonella-induced filament formation and bacterial growth within the late SCV. Our results reveal that the dynamic communication between the SCV and distinct host organelles affects both intracellular Salmonella localization and growth at successive steps of host cell invasion.