{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T23:55:16Z","timestamp":1790380516657,"version":"4.1.0"},"reference-count":60,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,3,10]],"date-time":"2022-03-10T00:00:00Z","timestamp":1646870400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p><jats:italic>Porphyromonas gingivalis<\/jats:italic>, a keystone periodontal pathogen, has emerged as a risk factor for systemic chronic diseases, including non-alcoholic fatty liver disease (NAFLD). To clarify the mechanism by which this pathogen induces such diseases, we simultaneously analyzed the transcriptome of intracellular <jats:italic>P. gingivalis<\/jats:italic> and infected host cells <jats:italic>via<\/jats:italic> dual RNA sequencing. Pathway analysis was also performed to determine the differentially expressed genes in the infected cells. Further, the infection-induced notable expression of <jats:italic>P. gingivalis livk<\/jats:italic> and <jats:italic>livh<\/jats:italic> genes, which participate in branched-chain amino acid (BCAA) transfer, was also analyzed. Furthermore, given that the results of recent studies have associated NAFLD progression with elevated serum BCAA levels, which reportedly, are upregulated by <jats:italic>P. gingivalis<\/jats:italic>, we hypothesized that this pathogen may induce increases in serum BCAA levels and exacerbate liver injury <jats:italic>via livh\/livk<\/jats:italic>. To verify this hypothesis, we constructed <jats:italic>P. gingivalis livh\/livk<\/jats:italic>-deficient strains (<jats:italic>\u0394livk<\/jats:italic>, <jats:italic>\u0394livh<\/jats:italic>) and established a high-fat diet (HFD)-fed murine model infected with <jats:italic>P. gingivalis<\/jats:italic>. Thereafter, the kinetic growth and exopolysaccharide (EPS) production rates as well as the invasion efficiency and <jats:italic>in vivo<\/jats:italic> colonization of the mutant strains were compared with those of the parental strain. The serum BCAA and fasting glucose levels of the mice infected with either the wild-type or mutant strains, as well as their liver function were also further investigated. It was observed that <jats:italic>P. gingivalis<\/jats:italic> infection enhanced serum BCAA levels and aggravated liver injury in the HFD-fed mice. Additionally, <jats:italic>livh<\/jats:italic> deletion had no effect on bacterial growth, EPS production, invasion efficiency, and <jats:italic>in vivo<\/jats:italic> colonization, whereas the <jats:italic>\u0394livk<\/jats:italic> strain showed a slight decrease in invasion efficiency and <jats:italic>in vivo<\/jats:italic> colonization. More importantly, however, both the <jats:italic>\u0394livk<\/jats:italic> and <jats:italic>\u0394liv<\/jats:italic>h strains showed impaired ability to upregulate serum BCAA levels or exacerbate liver injury in HFD-fed mice. Overall, these results suggested that <jats:italic>P. gingivalis<\/jats:italic> possibly aggravates NAFLD progression in HFD-fed mice by increasing serum BCAA levels, and this effect showed dependency on the bacterial BCAA transport system.<\/jats:p>","DOI":"10.3389\/fcimb.2022.776996","type":"journal-article","created":{"date-parts":[[2022,3,10]],"date-time":"2022-03-10T15:10:22Z","timestamp":1646925022000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["Porphyromonas gingivalis Induces Increases in Branched-Chain Amino Acid Levels and Exacerbates Liver Injury Through livh\/livk"],"prefix":"10.3389","volume":"12","author":[{"given":"Leng","family":"Wu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huimin","family":"Bai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingtong","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Wei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chengcheng","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yafei","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,3,10]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1038","DOI":"10.1016\/j.metabol.2015.12.012","article-title":"The Multiple-Hit Pathogenesis of Non-Alcoholic Fatty Liver Disease (NAFLD)","volume":"65","author":"Buzzetti","year":"2016","journal-title":"Metabolism"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mec.2020.e00136","article-title":"Systematic Engineering of Branch Chain Amino Acid Supply Modules for the Enhanced Production of Bacitracin From Bacillus Licheniformis","volume":"11","author":"Cai","year":"2020","journal-title":"Metab. 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