Translocation of Yersinia entrocolitica across reconstituted intestinal epithelial monolayers is triggered by Yersinia invasin binding to beta1 integrins apically expressed on M-like cells

Détails

ID Serval
serval:BIB_CAEDDE65C90D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Translocation of Yersinia entrocolitica across reconstituted intestinal epithelial monolayers is triggered by Yersinia invasin binding to beta1 integrins apically expressed on M-like cells
Périodique
Cellular Microbiology
Auteur(s)
Schulte  R., Kerneis  S., Klinke  S., Bartels  H., Preger  S., Kraehenbuhl  J. P., Pringault  E., Autenrieth  I. B.
ISSN
1462-5814 (Print)
Statut éditorial
Publié
Date de publication
04/2000
Volume
2
Numéro
2
Pages
173-85
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Apr
Résumé
Yersinia enterocolitica cross the intestinal epithelium via translocation through M cells, which are located in the follicle-associated epithelium (FAE) of Peyer's patches (PP). To investigate the molecular basis of this process, studies were performed using a recently developed in vitro model, in which the enterocyte-like cell line Caco-2 and PP lymphocytes are co-cultured in order to establish FAE-like structures including M cells. Here, we demonstrate that Y. enterocolitica does not adhere significantly to the apical membrane of differentiated enterocyte-like Caco-2 cells that express binding sites for Ulex europaeus agglutinin (UEA)-1. In contrast, Y. enterocolitica adhered to, and was internalized by, cells that lacked UEA-1 binding sites and displayed a disorganized brush border. These cells were considered to be converted to M-like cells. Further analysis revealed that part of these cells expressed beta1 integrins at their apical surface and, as revealed by comparison of wild-type and mutant strains, interacted with invasin of Y. enterocolitica. Consistently, anti-beta1 integrin antibodies significantly inhibited internalization of inv-expressing yersiniae. Experiments with Yersinia mutant strains deficient in YadA or Yop secretion revealed that these virulence factors play a minor role in this process. After internalization, yersiniae were transported within LAMP-1-negative vacuoles to, and released at, the basal surface. Internalization and transport of yersiniae was inhibited by cytochalasin D, suggesting that F-actin assembly is required for this process. These results provide direct evidence that expression of beta1 integrins at the apical surface of M cells enables interaction with the invasin of Y. enterocolitica, and thereby initiates internalization and translocation of bacteria.
Mots-clé
*Adhesins, Bacterial Antigens, CD29/*metabolism Bacterial Adhesion Bacterial Proteins/*metabolism Caco-2 Cells Coculture Techniques Epithelial Cells/*microbiology Humans Intestinal Mucosa/cytology/*microbiology Lymphocytes/microbiology Microscopy, Electron Microscopy, Fluorescence Yersinia Infections/microbiology Yersinia enterocolitica/genetics/*pathogenicity/physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 16:06
Dernière modification de la notice
09/05/2019 1:16
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