Porphyromonas gingivalis aggravates colitis via a gut microbiota-linoleic acid metabolism-Th17/Treg cell balance axis
Jia L, Jiang Y, Wu L, Fu J, Du J, Luo Z, Guo L, Xu J, Liu Y
Nature communications · 161 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Animales
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Natural Science Foundation of China
- Universidad u hospital
- Capital Medical University
- Gobierno
- Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support
- Gobierno
- Beijing Municipal Administration of Hospitals
- Gobierno
- National Natural Science Foundation of China (National Science Foundation of China)
- Subvenciones
- National Natural Science Foundation of China (81974149); National Natural Science Foundation of China (82101009); National Natural Science Foundation of China (DFL20181501); Beijing Municipal Administration of Hospitals (81991504); Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support (81991504); National Natural Science Foundation of China (QML20181501); Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support (QML20181501); National Natural Science Foundation of China (82122015); Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support (DFL20181501); Beijing Municipal Administration of Hospitals (DFL20181501); National Natural Science Foundation of China (2022YFC2504200); Beijing Municipal Administration of Hospitals (81974149); Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support (81974149); Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support (ZYLX202121); National Natural Science Foundation of China (81991504); Beijing Municipal Administration of Hospitals (QML20181501)
Según 5 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2024-02-22 · Nat Commun · vol. 15 · número 1 · pág. 1617
- Editorial
- Nature Portfolio
- Citado
- 199 citas · más que el 100% de estudios similares · 35.2× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 69 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Gut microbiota and health · Immune Response and Inflammation · Oral microbiology and periodontitis research
- Palabras clave
- Porphyromonas gingivalis, Gut flora, Dysbiosis, Colitis, Immunology, Periodontitis, Inflammation, Microbiome, Biology, Immune system, Medicine, Internal medicine, Bioinformatics
- MeSH
- animals, mice, inbred c57bl, humans, mice, porphyromonas gingivalis, colitis, inflammatory bowel diseases, periodontitis, inflammation, linoleic acid, t-lymphocytes, regulatory, th17 cells, gastrointestinal microbiome
9 autores
- Jia Lü🇨🇳Capital Medical University
- Yiyang Jiang🇨🇳Capital Medical University
- Lili Wu🇨🇳Capital Medical University
- Jingfei Fu🇨🇳Capital Medical University
- Juan Du🇨🇳Capital Medical University
- Zhenhua Luo🇨🇳Capital Medical University
- Lijia Guo🇨🇳Capital Medical University
- Junji Xu🇨🇳🇵🇱 · autor de correspondenciaCapital Medical University; Cells Therapy (Poland)
- Yi Fan Liu🇨🇳🇵🇱 · autor de correspondenciaCapital Medical University; Cells Therapy (Poland)
Resumen
El texto original del estudio, en el idioma en que se publicó.
Periodontitis is closely related to inflammatory bowel disease (IBD). An excessive and non-self-limiting immune response to the dysbiotic microbiome characterizes the two. However, the underlying mechanisms that overlap still need to be clarified. We demonstrate that the critical periodontal pathogen Porphyromonas gingivalis (Pg) aggravates intestinal inflammation and Th17/Treg cell imbalance in a gut microbiota-dependent manner. Specifically, metagenomic and metabolomic analyses shows that oral administration of Pg increases levels of the Bacteroides phylum but decreases levels of the Firmicutes, Verrucomicrobia, and Actinobacteria phyla. Nevertheless, it suppresses the linoleic acid (LA) pathway in the gut microbiota, which was the target metabolite that determines the degree of inflammation and functions as an aryl hydrocarbon receptor (AHR) ligand to suppress Th17 differentiation while promoting Treg cell differentiation via the phosphorylation of Stat1 at Ser727. Therapeutically restoring LA levels in colitis mice challenged with Pg exerts anti-colitis effects by decreasing the Th17/Treg cell ratio in an AHR-dependent manner. Our study suggests that Pg aggravates colitis via a gut microbiota-LA metabolism-Th17/Treg cell balance axis, providing a potential therapeutically modifiable target for IBD patients with periodontitis.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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