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Infect. Immun., 07 1996, 2752-2764, Vol 64, No. 7
PJ Sansonetti, J Arondel, JR Cantey, MC Prevost and M Huerre
In order to invade the colonic mucosa, the bacterial pathogen Shigella
flexneri must find a site of entry. Experiments with the rabbit ligated
intestinal loop model described here confirm that M cells of the
follicle-associated epithelium (FAE) that covers lymphoid structures of the
Peyer's patches represent a major site of entry for invasive
microorganisms. In addition, in an isogenic Shigella background, expression
of an adhesive phenotype, or of an invasive phenotype, is required for
bacteria to efficiently colonize the FAE. A nonadhesive, noninvasive mutant
barely interacted with FAE. Adhesive and invasive strains induced dramatic
but different alterations on FAE. Invasive strain M90T caused major
inflammation-mediated tissue destruction after 8 h of infection. Adhesive
strain BS15 caused limited inflammation, but major architectural changes,
characterized by an increase in the size of M cells that became stretched
over large pockets containing an increased number of mononuclear cells,
were observed. M cells progressively occupied large surface areas of the
FAE at the expense of enterocytes. This contributed to enterocytes losing
contact with the lumen. These experiments demonstrate that various
remodeling patterns may occur in Peyer's patches in response to bacterial
pathogens, depending on the virulence phenotype expressed by the pathogenic
strain.
Copyright © 1996, American Society for Microbiology
Infection of rabbit Peyer's patches by Shigella flexneri: effect of adhesive or invasive bacterial phenotypes on follicle-associated epithelium
Unite de Pathogenie Microbienne Moleculaire, U389 INSERM, Institut Pasteur, Paris. psanson@pasteur.fr
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