The biological role of invasin during a Yersinia enterocolitica infection.

Epidemiological data suggest that the ability to invade the intestinal epithelium of mammals is an essential virulence determinant of Yersinia enterocolitica. The chromosomally encoded Y. enterocolitica 8081v invasion gene, inv, was disrupted to assess its role in pathogenesis. The inv mutant was unable to invade cultured epithelial cells as efficiently as wild type. Furthermore, when mice were infected intragastrically, the inv mutant was extremely deficient at penetrating the murine intestinal epithelium. Analysis of the course of infection showed that the inv mutant had distinct differences relative to wild type in the distribution of visible infectious foci and in tissue colonization; however, the mutant and wild-type strains had similar median lethal doses for both orally and intraperitoneally infected mice. The invasion defect of the inv mutant was fully complemented in vitro and in vivo by introduction of the wild-type inv gene in trans. The inv gene product, invasin, appears to play a vital role in promoting entry during the initial stage of infection. During the subsequent establishment of a systemic infection, invasin may be of secondary importance, since the Y. enterocolitica inv mutant was as proficient as wild-type at causing a fatal infection in mice. The possible role of invasin in a naturally occurring Y. enterocolitica infection is discussed.