Previous Article | Next Article ![]()
Infect. Immun., Dec 1997, 5309-5319, Vol 65, No. 12
M Lecuit, H Ohayon, L Braun, J Mengaud and P Cossart
Listeria monocytogenes can use two different surface proteins, internalin
(InlA) and InlB, to invade mammalian cells. The exact role of these
invasiveness factors in vivo remains to be determined. In cultured cells,
InlA is necessary to promote Listeria entry into human epithelial cells,
such as Caco-2 cells, whereas InlB is necessary to promote Listeria
internalization in several other cell types, including hepatocytes,
fibroblasts, and epithelioid cells, such as Vero, HeLa, CHO, or Hep-2
cells. We have recently reported that the InlA receptor on Caco-2 cells is
the cell adhesion molecule E-cadherin and demonstrated that nonpermissive
fibroblasts become permissive for internalin-mediated entry when
transfected with the gene coding for LCAM, the chicken homolog of the human
E-cadherin gene. In this study, we demonstrate for the first time that the
internalin protein alone is sufficient to promote internalization into
cells expressing its receptor. Indeed, internalin confers invasiveness to
both Enterococcus faecalis and internalin-coated latex beads. As shown by
transmission electron microscopy, these beads were phagocytosed via a
"zipper" mechanism similar to that observed during the
internalin-E-cadherin- mediated entry of Listeria. Moreover, a functional
analysis of internalin demonstrates that its amino-terminal region,
encompassing the leucine-rich repeat (LRR) region and the inter-repeat (IR)
region, is necessary and sufficient to promote bacterial entry into cells
expressing its receptor. Several lines of evidence suggest that the LRR
region would interact directly with E-cadherin, whereas the IR region would
be required for a proper folding of the LRR region.
Copyright © 1997, American Society for Microbiology
Internalin of Listeria monocytogenes with an intact leucine-rich repeat region is sufficient to promote internalization
Unite des Interactions Bacteries-Cellules, Institut Pasteur, Paris, France.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»