Figure 3.

Virulence factors and related effects in P. gingivalis OMVs. (1) P. gingivalis OMVs can be internalized into cells by an actin-mediated pathway that utilizes host receptors, especially α5β1-integrin, which is controlled by PI3K and depends on caveolin, dynamin, and Rac1. (2) P. gingivalis OMVs can be internalized into cells through the fimbria-dependent lipid raft pathway, which is dependent on PI3K and Rac1, and involves various regulatory GTPases. (3) P. gingivalis OMVs can exert virulence by affecting different receptors on the host cell surface, such as activating PRR receptors and degrading TfR receptors. (4–6) P. gingivalis OMVs can activate or degrade a variety of biologically active substances in host cells, inhibit cell proliferation, promote glycolysis, apoptosis, and cause host cells to produce a variety of inflammatory factors thereby promoting the formation of an inflammatory environment.