Periodontal disease is of established aetiology in which polymicrobial
synergistic ecology has become dysbiotic under the influence of
Porphyromonas gingivalis. Following breakdown of the host’s protective
oral tissue barriers, P. gingivalis migrates to developing inflammatory
pathologies that associate with Alzheimer’s disease (AD). Periodontal
disease is a risk factor for cardiovascular disorders (CVD), type II
diabetes mellitus (T2DM), AD and other chronic diseases, whilst T2DM
exacerbates periodontitis. This study analysed the relationship between
the P. gingivalis/host interactome and the genes identified in
genome-wide association studies (GWAS) for the aforementioned conditions
using data from GWASdb (P<1E-03) and, in some cases, from the
NCBI/EBI GWAS database (P< 1E-05). Gene expression data from
periodontitis or P. gingivalis microarray was compared to microarray
datasets from the AD hippocampus and/or from carotid artery plaques. The
results demonstrated that the host genes of the P. gingivalis
interactome were significantly enriched in genes deposited in GWASdb
genes related to cognitive disorders, AD and dementia, and its co-morbid
conditions T2DM, obesity, and CVD. The P. gingivalis/host interactome
was also enriched in GWAS genes from the more stringent NCBI-EBI
database for AD, atherosclerosis and T2DM. The misregulated genes in
periodontitis tissue or P. gingivalis infected macrophages also matched
those in the AD hippocampus or atherosclerotic plaques. Together, these
data suggest important gene/environment interactions between P.
gingivalis and susceptibility genes or gene expression changes in
conditions where periodontal disease is a contributory factor.
synergistic ecology has become dysbiotic under the influence of
Porphyromonas gingivalis. Following breakdown of the host’s protective
oral tissue barriers, P. gingivalis migrates to developing inflammatory
pathologies that associate with Alzheimer’s disease (AD). Periodontal
disease is a risk factor for cardiovascular disorders (CVD), type II
diabetes mellitus (T2DM), AD and other chronic diseases, whilst T2DM
exacerbates periodontitis. This study analysed the relationship between
the P. gingivalis/host interactome and the genes identified in
genome-wide association studies (GWAS) for the aforementioned conditions
using data from GWASdb (P<1E-03) and, in some cases, from the
NCBI/EBI GWAS database (P< 1E-05). Gene expression data from
periodontitis or P. gingivalis microarray was compared to microarray
datasets from the AD hippocampus and/or from carotid artery plaques. The
results demonstrated that the host genes of the P. gingivalis
interactome were significantly enriched in genes deposited in GWASdb
genes related to cognitive disorders, AD and dementia, and its co-morbid
conditions T2DM, obesity, and CVD. The P. gingivalis/host interactome
was also enriched in GWAS genes from the more stringent NCBI-EBI
database for AD, atherosclerosis and T2DM. The misregulated genes in
periodontitis tissue or P. gingivalis infected macrophages also matched
those in the AD hippocampus or atherosclerotic plaques. Together, these
data suggest important gene/environment interactions between P.
gingivalis and susceptibility genes or gene expression changes in
conditions where periodontal disease is a contributory factor.
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