Porphyromonas gingivalis Strain Specific Interactions with Human Coronary Artery Endothelial Cells: A Comparative Study

Abstract

Both epidemiologic and experimental findings suggest that infection with Porphyromonas gingivalis exacerbates progression of atherosclerosis. As P. gingivalis exhibits significant strain variation, it is reasonable that different strains possess different capabilities and/or mechanisms by which they promote atherosclerosis. Using P. gingivalis strains that have been previously evaluated in the ApoE null atherosclerosis model, we assessed the ability of W83, A7436, 381, and 33277 to adhere, invade, and persist in human coronary artery endothelial (HCAE) cells. W83 and 381 displayed an equivalent ability to adhere to HCAE cells, which was significantly greater than both A7436 and 33277 (P<0.01). W83, 381, and 33277 were more invasive than A7436 (P<0.0001). However, only W83 and A7436 were able to remain viable up to 48 hours in HCAE cell cultures, whereas 381 was cleared by 48 hours and 33277 was cleared by 24 hours. These differences in persistence were in part due to strain specific differences in intracellular trafficking. Both W83 and 381 trafficked through the autophagic pathway, but not A7436 or 33277. Internalized 381 was the only strain that was dependent upon the autophagic pathway for its survival. Finally, we assessed the efficacy of these strains to activate HCAE cells as defined by production of IL-6, IL-8, IL-12p40, MCP-1, RANTES, TNF-α, and soluble adhesion molecules (sICAM-1, sVCAM-1, and sE-selectin). Only moderate inflammation was observed in cells infected with either W83 or A7436, whereas cells infected with 381 exhibited the most profound inflammation, followed by cells infected with 33277. These results demonstrate that virulence mechanisms among different P. gingivalis strains are varied and that pathogenic mechanisms identified for one strain are not necessarily applicable to other strains.

Porphyromonas gingivalisand adverse pregnancy outcome

“…It is already well established that P. gingivalis strains exhibit different degrees of pathogenicity based on their ability to invade host cells, disseminate to various organ/tissue sites, and induce disease [77,[98][99][100]. This phenomenon also appears to occur in APOs, as indicated by experimental infection in pregnant rats [48].…”

“…As already mentioned, dMΦ also appear to have a role in spiral artery remodeling and trophoblast migration, typically bear markers associated with tissue remodeling and phagocytosis of debris, and have recently been divided into two subsets: one more regulatory, + decidual macrophages (B). P. gingivalis (red) was detected with a rabbit polyclonal antibody to whole cell W83 [6,77], uNK cells were identified with mouse monoclonal antibody clone ANK61 to NK cell activation structure, decidual macrophages were labeled with anti-CD68 mouse clone ED1antibody (Abcam®, Cambridge, MA), and nuclei (blue) were stained with DAPI (results have not been published elsewhere).…”

Porphyromonas gingivalisin periodontal pockets and heart valves

“…What is more, treatment of periodontal diseases, including a control of periodontal infections, results in improved levels of markers of systemic inflammation and endothelial dysfunction. [22][23][24] The ability of oral pathogens to colonize coronary atheromatous plaque has already been confirmed by studies showing the 27 It has been reported that P. gingivalis accelerated atheroma formation, [28][29][30] caused an increase in systemic inflammatory marker levels, 20,21 invaded endothelium and vascular smooth muscle cells, 31,32 and appeared to alter endothelial function. 33,34 P. gingivalis activates endothelial cells and upregulates various adhesion molecules, and thus, increases the likelihood of macrophage diapedesis and subsequent conversion to foam cells.…”

“…35 However, the virulence mechanisms are different for various P. gingivalis strains and a detailed examination of these processes needs to be performed. 32 In this study, the assessment of the presence of P. gingivalis DNA in cardiac valves in relation to its presence in periodontal pockets was performed. Overall, in our research, severe periodontitis was diagnosed only in six patients.…”

Representation of microorganisms of subgingival plaque at different degrees of periodontium tissue inflamation and destruction

“…Zbog toga se smatra da je parodontopatija zajednički naziv za familiju sličnih oboljenja koja se međusobno razlikuju po etiologiji, toku i odgovoru na terapiju, ali dele iste puteve tkivne destrukcije [13]. Klinička slika je rezultat kompleksnih reakcija između dejstva mikroorganizama, zajedničkih događaja ("shared events") i modifikatora bolesti [14].…”