Porphyromonas gingivalis, a Gram-negative bacterial pathogen and natural component of the oral mucosal microbiome, is the causative agent of periodontal disease (i.e., gingivitis), which can lead to periodontal bone loss (Fiehn et al. 1992). This pathogen has also been involved in cardiovascular disease, pulmonary infections and atherosclerosis. Gingival epithelial cells are among the first host cells colonized by P. gingivalis. P. gingivalis invades and replicates in human endothelial cells, producing an array of potential virulence factors including extracellular proteases. The binding of the bacterial fimbriae to the host cellular b1-integrin receptor is required for invasion (Deshpande et al. 1998; reviewed by Yilmaz 2008) and for activation of endothelial cells, which leads to the development of atherogenesis (Takahashi et al. 2006). Activation of signaling molecules and actin rearrangements are key events upon the interaction of the bacterium with plasma membrane components. It is interesting to note that, as described for Legionella, lipid rafts also seem to be involved in P. gingivalis internalization. The protein caveolin 1 colocalizes with P. gingivalis, and reduction of plasma membrane cholesterol or knockdown of caveolin 1 decreases bacterial uptake (Tamai et al. 2005). However, it is not known if the interaction with lipids rafts is important for the subsequent connection with the autophagy pathway, as has been previously demonstrated for L. pneumophila (Amer and Swanson 2005).
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