INVASIN-DEPENDENT AND INVASIN-INDEPENDENT PATHWAYS FOR TRANSLOCATION OF YERSINIA-PSEUDOTUBERCULOSIS ACROSS THE PEYERS PATCH INTESTINAL EPITHELIUM

Authors
Citation
A. Marra et Rr. Isberg, INVASIN-DEPENDENT AND INVASIN-INDEPENDENT PATHWAYS FOR TRANSLOCATION OF YERSINIA-PSEUDOTUBERCULOSIS ACROSS THE PEYERS PATCH INTESTINAL EPITHELIUM, Infection and immunity, 65(8), 1997, pp. 3412-3421
Citations number
40
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
65
Issue
8
Year of publication
1997
Pages
3412 - 3421
Database
ISI
SICI code
0019-9567(1997)65:8<3412:IAIPFT>2.0.ZU;2-I
Abstract
Yersinia pseudotuberculosis initiates systemic disease after transloca tion across the intestinal epithelium. Three Y. pseudotuberculosis fac tors, previously identified by their ability to promote association wi th cultured cells, were evaluated for their relative roles in transloc ation, To this end, mutants defective for invasin, YadA, or pH 6 antig en were tested for movement from the intestinal lumen into the subepit helium. Within 45 min after introduction of bacteria into the lumen, w ild-type bacteria were found in the Peyer's patch, Mutants expressing defective invasin derivatives were unable to promote efficient translo cation into the Peyer's patch and instead colonized on the luminal sur face of the intestinal epithelium. In particular, a translocation defe ct was observed in a Y. pseudotuberculosis strain that expressed an up take-defective invasin protein retaining considerable receptor binding activity, To attempt to reduce binding to luminal mucus, Y. pseudotub erculosis yadA and inv yadA strains were analyzed, Both strains had re duced mucus binding, with the inv yadA mutant revealing an alternate u ptake pathway that was invasin independent, A mutant defective in the production of the pH 6 antigen adhesin also showed reduced binding to luminal mucus, with specific localization of bacteria in M cells, Thes e results indicate that Y. pseudotuberculosis adhesive factors control the site of bacterial interaction within the intestinal environment a nd that loss of one factor causes drastic changes in the preferred sit e of localization of the bacterium in this locale.