Figure 2. Current model of P. gingivalis interactions with gingival epithelial cells. Interactions between P. gingivalis fimbriae, gingipains, and other potential adhesins with various epithelial cell-surface receptors (PAR-1/2, TLR2, integrins) lead to the activation of epithelial cell signaling pathways and the modulation of gene expression. The entry of P. gingivalis into epithelial cells is associated with the phosphorylation/dephosphorylation of signaling molecules such as MAP kinases, the modulation of calcium influx, and the re-arrangement of the cell cytoskeleton. Interactions of fimbriae with integrins initiate down-stream signaling events, including the formation of focal adhesion molecules such as FAK/paxillin. The intracellular localization of gingipains can interfere with the pathways of the focal adhesion molecules FAK/paxillin and MAP kinase. This model has been adapted from a model proposed by Lamont and Jenkinson (1998). See text for references. Abbreviations: Ca++, calcium; ERK, extracellular signal-regulated kinase; GTP, guanosine triphosphate; IkB, inhibitory factor; ILß, interleukin; JNK, c-Jun N-terminal; MAPKKK, mitogen-activated protein kinase kinase kinase; MEK, extracellular signal-regulated kinase activator kinase; NF-B, nuclear transcriptional factor; PAR, protease-activated receptor; RAS, small-GTPase; and TLR, Toll-like receptor.