Oral Administration of Porphyromonas gingivalis Alters the Gut Microbiome and Serum Metabolome

This research was originally published in 2018 by Tamotsu Kato, Kyoko Yamazaki, Mayuka Nakajima, Yasuhiro Date, Jun Kikuchi, Koji Hase, Hiroshi Ohno, Kazuhisa Yamazakia.

We have curated this article as a reference point for The Larkin Protocol.

ABSTRACT:

Periodontal disease induced by periodontopathic bacteria likePorphy-romonas gingivalisis demonstrated to increase the risk of metabolic, inflammatory,and autoimmune disorders. Although precise mechanisms for this connection havenot been elucidated, we have proposed mechanisms by which orally administeredperiodontopathic bacteria might induce changes in gut microbiota composition, bar-rier function, and immune system, resulting in an increased risk of diseases charac-terized by low-grade systemic inflammation. Accumulating evidence suggests a pro-found effect of altered gut metabolite profiles on overall host health. Therefore, it ispossible thatP. gingivaliscan affect these metabolites. To test this, C57BL/6 micewere administered withP. gingivalisW83 orally twice a week for 5 weeks and com-pared with sham-inoculated mice. The gut microbial communities were analyzed bypyrosequencing the 16S rRNA genes. Inferred metagenomic analysis was used to de-termine the relative abundance of KEGG pathways encoded in the gut microbiota.Serum metabolites were analyzed using nuclear magnetic resonance (NMR)-basedmetabolomics coupled with multivariate statistical analyses. Oral administration ofP.gingivalisinduced a change in gut microbiota composition. The distributions of met-abolic pathways differed between the two groups, including those related to aminoacid metabolism and, in particular, the genes for phenylalanine, tyrosine, and trypto-phan biosynthesis. Also, alanine, glutamine, histidine, tyrosine, and phenylalaninewere significantly increased in the serum ofP. gingivalis-administered mice. In addi-tion to altering immune modulation and gut barrier function, oral administration ofP. gingivalisaffects the host’s metabolic profile. This supports our hypothesis regard-ing a gut-mediated systemic pathology resulting from periodontal disease.

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