Porphyromonas gingivalis HSP60 peptides have distinct roles in the development of atherosclerosis

The therapeutic potential of regulatory T lymphocytes in periodontitis: A systematic review

“…Next, immunization with the peptide 14 from the P. gingivalis heat‐shock protein (Pg14) resulted in an increase in the percentage of CD4 + CD25 + Foxp3 + Tregs (~2.6‐2.9 times) and in a significant increase of Foxp3 expression (1.3 times higher) in the Pg14‐vaccinated group compared to all other groups ( P < 0.05) . Nevertheless, the same intervention with Pg19 resulted in a 6.2 times higher increment of CD4 + IFN‐γ + Th1 lymphocytes, 3.3 times higher IL‐6 concentration and 4.3 times higher IFN‐γ expression in the Pg19‐vaccinated group in comparison with the control group ( P < 0.05), in the spleen . Moreover, immunization with a pathogen‐derived heat‐shock protein (GroEL) from P. gingivalis showed a significant increase in the percentage of IFN‐γ–producing CD4 + Foxp3 + cells (M = 3.3, SD = 0.2 vs M = 0.4, SD = 0.2, P < 0.05), IL‐10–producing CD4 + Foxp3 + cells (M = 3.4, SD = 0.1 vs M = 0.6, SD = 0.2, P < 0.05) and IL‐10–producing CD4 + Foxp3 − Tregs (M = 0.9, SD = 0.1 vs M = 0.3, SD = 0.1, P < 0.05) in the GroEL‐vaccinated group in comparison with control, detected in the submandibular gland.…”

“…The murine experimental models were used in 100% of the studies, from which the mouse model was the most frequently used animal model (76.2%) . In the studies using mice, 10 studies used the C57BL/6 strain, four studies used the BALB/c strain, and three studies did not specify the animal strain used . In addition, seven studies used only wild‐type mice, nine studies used both wild‐type and knockout mice, and one study used wild‐type, knockout and the 10BiT mice, corresponding to a IL‐10 reporter animal.…”

Pep19 drives epitope spreading in periodontitis and periodontitis‐associated autoimmune diseases

“…Based on our series observations (14,15,17,19), we hypothesized that the Pep19 may be a dominant epitope from which the epitope-specific immune response to subdominant epitopes may diversify sequentially into autoimmune responses directed at human neoepitopes in P. gingivalis-induced periodontitis and autoimmune diseases. To clarify this phenomenon and to identify the mechanism to support the hypothesis, a study has been devised for two independent investigations; a cross-sectional analysis on clinical subjects and a prospective analysis on experimental periodontitis, each being subdivided further into two additional independent observations.…”

Correlation is not causation: Probable role of immunization with bacillus almetteguerin vaccine in atherogenesis

“…ese latter authors reported that the aggregate burden ("infectious burden") of these chronic infections, rather than the effects of a single organism, might contribute to atherosclerosis and its complications. Beyond the abovementioned infectious agents, a large number of infectious agents have been linked with the pathobiology of atherosclerosis; examples include Porphyromonas gingivalis, in uenza A virus, herpes virus, hepatitis C virus, cytomegalovirus, human immunode ciency virus (12)(13)(14) and fungi (15; also 16, 17 for fungalbionic hypothesis of gout and related diseases including atherosclerosis). ese can mediate the T-cell sensitization required for the production of antibodies.…”

“…We based this proposal on: (i) atherosclerosis is present even in children (six months after birth) (19), (ii) every newborn receives BCG and other approximately 15 compulsory applications of immune products during the rst two years of life, (iii) all cell types involved in atherogenesis express constitutive and/or inducible HSP60 (8-11), (iv) HSP60 is a component of vaccines and adjuvants (4), (v) infections are the most common diseases of early childhood, (vi) HSP60 are existing in infectious agents (6,13,15), (vii) antibodies against HSP60 circulate in the blood of patients with atherosclerosis (5,20), (viii) experimental application of HSP60 triggers atherogenesis (3,21,22), (ix) BCG immunization induces atherosclerotic lesion in rabbits (22, 23) (x) Mycobacteria modulate proteins of host endothelial cells (24) and macrophages (25) to enter and persist within these cells Altogether, we suggest that (i) in a manner similar to molecular Koch postulates, the atherogenic potential of HSP60/ BCG immunization should be thoroughly evaluated (see 26), and (ii) it is reasonable to try to invent immune products (vaccines) that will serve to prevent disease, without casting a shadow.…”