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Infect Immun. 1991 January; 59(1): 253-260

Interactions between Yersinia enterocolitica and rabbit ileal mucus: growth, adhesion, penetration, and subsequent changes in surface hydrophobicity and ability to adhere to ileal brush border membrane vesicles.

A Paerregaard, F Espersen, O M Jensen and M Skurnik

Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.

ABSTRACT

Interactions between Yersinia enterocolitica and rabbit ileal mucus were examined. Strains carrying the Yersinia virulence plasmid, pYV, adhered to crude mucus but not to intestinal luminal contents that had been immobilized on polystyrene. Using an Y. enterocolitica O:9 mutant in which the yadA gene (formerly called yopA), encoding the high-molecular-weight outer membrane protein YadA (formerly called protein P1 or Yop1), had been inactivated and an Escherichia coli strain carrying the cloned yadA gene, we demonstrated that the ability to adhere to mucus correlated closely to expression of YadA. Thereafter, we evaluated possible consequences of binding between pYV-carrying Y. enterocolitica O:3 strains and constituents in the mucus layer. pYV-carrying strains were able to multiply at a high rate in mucus but not in luminal contents, and the ability to adhere to mucus could therefore facilitate bacterial colonization of the mucosa. However, we also showed in vitro that mucus acted as a barrier for a mucus-adherent, pYV-carrying Y. enterocolitica strain. Furthermore, penetration through, or preincubation with, mucus reduced subsequent adhesion of the pYV-carrying strain to brush border membrane vesicles without simultaneously causing bacterial aggregation. Preincubation with mucus also changed the bacterial surface of the same strain from hydrophobic to hydrophilic. Immunoglobulins present in mucus did not seem to be of importance for our observations. Interaction of Y. enterocolitica with intestinal mucus may thus reflect a host defense mechanism that reduces the pYV-mediated adhesion to the epithelial cell membrane, possibly by rendering the bacteria less hydrophobic.


Infect Immun. 1991 January; 59(1): 253-260




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