Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This content was analysed in patients with chronic periodontitis and in control subjects. In periodontal disease, it was characterized by higher mean concentrations of glycine, proline, tyrosine and delta-aminovaleric acid than in controls (p less than 0.001). However, the range of values varied considerably in the two groups. There were differences between periodontitis and control samples in the proportions of proline to serine (p less than 0.01) and proline to glutamic acid and glutamine (p less than 0.05). Bacterial contamination and decomposition of salivary proteins is responsible for the elevated salivary levels of glycine, proline, tyrosine and delta-aminovaleric acid in the periodontal group.
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PMID:Free amino-acid content of wax-stimulated human whole saliva as related to periodontal disease. 348 59

The immunologic cross-reactivity between human fibronectin and Actinobacillus actinomycetemcomitans GroEL was examined. Analyses by SDS-PAGE/Western immunoblotting and ELISA showed that a polyclonal antibody directed against the purified GroEL protein of A. actinomycetemcomitans, but not against the Escherichia coli GroEL, cross-reacts with human fibronectin. No antigenic cross-reactivity was observed between anti-A. actinomycetemcomitans GroEL antibody and type IV collagen, another important constituent of the basement membrane. A comparative analysis of the amino acid sequences of A. actinomycetemcomitans GroEL and human fibronectin revealed eight instances of four-amino acid sequence homology between the two proteins. Six of these tetrapeptide sequences were also shared with E. coli GroEL, suggesting that the remaining two tetrapeptides, GQLI (Glycine-Glutamine-Leucine-Isoleucine) and TGLE (Threonine-Glycine-Leucine-Glutamic acid), may be associated with the epitope that the anti-A. actinomycetemcomitans GroEL antibody specifically recognizes. Reactivity between TGLE, but not GQLI, with anti-A. actinomycetemcomitans GroEL antibody was confirmed by a biospecific interaction analysis using a biosensor technology. Although additional investigations are required, the observed phenomenon may lead to an autoimmune response and thus contribute to tissue destruction during periodontitis.
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PMID:Antigenic cross-reactivity and sequence homology between Actinobacillus actinomycetemcomitans GroEL protein and human fibronectin. 1487 54

Periodontal disease induced by periodontopathic bacteria like Porphyromonas gingivalis is demonstrated to increase the risk of metabolic, inflammatory, and autoimmune disorders. Although precise mechanisms for this connection have not been elucidated, we have proposed mechanisms by which orally administered periodontopathic bacteria might induce changes in gut microbiota composition, barrier function, and immune system, resulting in an increased risk of diseases characterized by low-grade systemic inflammation. Accumulating evidence suggests a profound effect of altered gut metabolite profiles on overall host health. Therefore, it is possible that P. gingivalis can affect these metabolites. To test this, C57BL/6 mice were administered with P. gingivalis W83 orally twice a week for 5 weeks and compared with sham-inoculated mice. The gut microbial communities were analyzed by pyrosequencing the 16S rRNA genes. Inferred metagenomic analysis was used to determine the relative abundance of KEGG pathways encoded in the gut microbiota. Serum metabolites were analyzed using nuclear magnetic resonance (NMR)-based metabolomics coupled with multivariate statistical analyses. Oral administration of P. gingivalis induced a change in gut microbiota composition. The distributions of metabolic pathways differed between the two groups, including those related to amino acid metabolism and, in particular, the genes for phenylalanine, tyrosine, and tryptophan biosynthesis. Also, alanine, glutamine, histidine, tyrosine, and phenylalanine were significantly increased in the serum of P. gingivalis-administered mice. In addition to altering immune modulation and gut barrier function, oral administration of P. gingivalis affects the host's metabolic profile. This supports our hypothesis regarding a gut-mediated systemic pathology resulting from periodontal disease.IMPORTANCE Increasing evidence suggest that alterations of the gut microbiome underlie metabolic disease pathology by modulating gut metabolite profiles. We have shown that orally administered Porphyromonas gingivalis, a representative periodontopathic bacterium, alters the gut microbiome; that may be a novel mechanism by which periodontitis increases the risk of various diseases. Given the association between periodontal disease and metabolic diseases, it is possible that P. gingivalis can affect the metabolites. Metabolite profiling analysis demonstrated that several amino acids related to a risk of developing diabetes and obesity were elevated in P. gingivalis-administered mice. Our results revealed that the increased risk of various diseases by P. gingivalis might be mediated at least in part by alteration of metabolic profiles. The findings should add new insights into potential links between periodontal disease and systemic disease for investigators in periodontal disease and also for investigators in the field of other diseases, such as metabolic diseases.
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PMID:Oral Administration of Porphyromonas gingivalis Alters the Gut Microbiome and Serum Metabolome. 3033 80