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Functional similarities between membrane blebs that mediate bacterial internalization and tumor metastasis have not previously been realized, and awareness of these similarities provides a new perspective on alterations in membrane properties that occur in association with tumor metastasis.
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We have previously proposed a model of C. jejuni-mediated invasion whereby this pathogen activates numerous components that comprise the focal complex, resulting in cytoskeletal rearrangement and bacterial internalization [ 19].
Several of these effectors stimulate Cdc42- and Rac1-dependent cytoskeletal changes that promote bacterial internalization.
Using enteric pathogens, adhesion molecule expression has been linked to bacterial internalization and to enterocyte differentiation.
This allows binding to Yersinia enterocolitica invasin and bacterial internalization into host intestinal epithelial cell.
Bacterial internalization is influenced by the surface properties of the leaf, including morphology, chemical constituents and metabolic activities (Leveau 2009).
The latter facilitate bacterial internalization [14], [15].
Actin polymerization leads to membrane ruffling, which promotes bacterial internalization.
In our study, Omp29 induced F-actin rearrangement and the resulting bacterial internalization in OBA9 cells (Fig. 4).
Surprisingly, infection of CEACAM1-transfected cells with Opa protein-negative meningococci resulted in bacterial internalization into the cells.
These findings suggested that Omp29-induced bacterial internalization is involved in PI3-kinase and Rho GTPase signaling in OBA9 cells.
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