YERSINIA INVASIN, A BACTERIAL BETA(1)-INTEGRIN LIGAND, IS A POTENT INDUCER OF LYMPHOCYTE MOTILITY AND MIGRATION TO COLLAGEN TYPE-IV AND FIBRONECTIN

The Yersinia pseudotuberculosis invasin protein was found to be a pote nt inducer of pseudopodia formation and chemotactic and haptotactic mi gration in human T lymphocytes. Checkerboard analysis confirmed that m igration was directional. The Yersinia invasin triggered migration of otherwise poorly migratory normal T cells on fibronectin and in partic ular on collagen type IV, and augmented the migration of leukemic T ce ll lines on these components. Invasin-induced lymphocyte migration was inhibited by staurosporin that selectively prevented pseudopodia form ation but, noteworthy, augmented adhesion. The motogenic and attractan t properties of invasin (Inv) were mediated via beta(1)-integrins, as shown by lack of effect of rnv on the motility of a beta(1)-integrin-n egative lymphoid cell line and inhibition of invasin-induced lymphocyt e motility by anti-beta(1) Abs. Inv was markedly more effective than t he extracellular matrix components fibronectin, collagen type IV, and laminin, which also interact with lymphocyte beta(1)-integrins, with r espect to induction of pseudopodia, chemotaxis, and haptotaxis. Thus, Yersinia invasin is a model ligand for induction of lymphocyte motilit y via beta(1)-integrins. The extraordinary capacity of Inv to trigger and guide T lymphocyte motility and potentiate lymphocyte migration to extracellular matrix components may be of pathogenetic significance f or the movement of lymphocytes to extraintestinal sites secondary to Y ersinia infection.