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© Pierre Gounon
Entrée de Listeria dans une cellule épithéliale (Grossissement X 10000). Image colorisée.
Publication : The Journal of cell biology

Role of lipid rafts in E-cadherin– and HGF-R/Met–mediated entry of Listeria monocytogenes into host cells

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of cell biology - 30 Aug 2004

Seveau S, Bierne H, Giroux S, Prévost MC, Cossart P

Link to Pubmed [PMID] – 15337781

J. Cell Biol. 2004 Aug;166(5):743-53

Listeria monocytogenes uptake by nonphagocytic cells is promoted by the bacterial invasion proteins internalin and InlB, which bind to their host receptors E-cadherin and hepatocyte growth factor receptor (HGF-R)/Met, respectively. Here, we present evidence that plasma membrane organization in lipid domains is critical for Listeria uptake. Cholesterol depletion by methyl-beta-cyclodextrin reversibly inhibited Listeria entry. Lipid raft markers, such as glycosylphosphatidylinositol-linked proteins, a myristoylated and palmitoylated peptide and the ganglioside GM1 were recruited at the bacterial entry site. We analyzed which molecular events require membrane cholesterol and found that the presence of E-cadherin in lipid domains was necessary for initial interaction with internalin to promote bacterial entry. In contrast, the initial interaction of InlB with HGF-R did not require membrane cholesterol, whereas downstream signaling leading to F-actin polymerization was cholesterol dependent. Our work, in addition to documenting for the first time the role of lipid rafts in Listeria entry, provides the first evidence that E-cadherin and HGF-R require lipid domain integrity for their full activity.

http://www.ncbi.nlm.nih.gov/pubmed/15337781