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Gut commensal Odoribacter splanchnicus alleviates hyperlipidemic periodontitis via the β-GPA-TLR4 axis

ABSTRACT:

Background: Hyperlipidemia is a well-established systemic metabolic disorder and a significant risk factor for periodontitis, a localized inflammatory condition; however, the precise mechanisms underpinning this comorbidity remain uncharacterized. Emerging evidence implicates the gut microbiota as a crucial mediator in the pathogenesis linking hyperlipidemia with periodontitis. Therefore, this study was designed to elucidate the causal role of the gut microbiota and its associated metabolic pathways in this interaction, with the ultimate goal of identifying microbiome-targeted therapeutic strategies.

Results: We found that hyperlipidemia exacerbates periodontal destruction by inducing specific gut microbiota dysbiosis. Notably, Odoribacter splanchnicus was significantly depleted in patients and mice with hyperlipidemic periodontitis (HPD). Through fecal microbiota transplantation, we established a causal link between HPD-associated gut microbiota and disease phenotypes. Oral administration of live O. splanchnicus attenuated periodontal bone loss and systemic metabolic dysfunction by remodeling the gut microbiome and upregulating the metabolite, β-guanidinopropionic acid (β-GPA). Crucially, direct supplementation with β-GPA similarly alleviated HPD phenotypes. Further mechanistic investigations revealed that β-GPA remotely inhibited the pro-inflammatory Toll-like receptor 4 (TLR4) signaling pathway in periodontal tissues.

Conclusions: Our findings establish the 'O. splanchnicus - β-GPA - TLR4' axis as a crucial protective pathway in HPD. This provides a mechanistic framework for the crosstalk between systemic metabolic disorders and local inflammatory diseases, representing an advance in microbiome-targeted therapeutic strategies for this complex comorbidity.

INSTRUMENT(S): Liquid Chromatography MS - alternating - reverse phase

PROVIDER: MTBLS13135 | MetaboLights | 2026-06-08

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13135_LC-MS_alternating_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13135_LC-MS_alternating_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	s_MTBLS13135.txt	Txt

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Project description:The effect of oral microbiota on the intestinal microbiota has garnered growing attention as a mechanism linking periodontal diseases to systemic diseases. However, the salivary microbiota is diverse and comprises numerous bacteria with a largely similar composition in healthy individuals and periodontitis patients. Thus, the systemic effects of small differences in the oral microbiota are unclear. In this study, we explored how health-associated and periodontitis-associated salivary microbiota differently colonized the intestine and their subsequent systemic effects by analyzing the hepatic gene expression and serum metabolomic profiles. The salivary microbiota was collected from a healthy individual and a periodontitis patient and gavaged into C57BL/6NJcl[GF] mice. Samples were collected five weeks after administration. Gut microbial communities were analyzed by 16S ribosomal RNA gene sequencing. Hepatic gene expression profiles were analyzed using a DNA microarray and quantitative polymerase chain reaction. Serum metabolites were analyzed by capillary electrophoresis time-of-flight mass spectrometry. The gut microbial composition at the genus level was significantly different between periodontitis-associated microbiota-administered (PAO) and health-associated oral microbiota-administered (HAO) mice. The hepatic gene expression profile demonstrated a distinct pattern between the two groups, with higher expression of Neat1, Mt1, Mt2, and Spindlin1, which are involved in lipid and glucose metabolism. Disease-associated metabolites such as 2-hydroxyisobutyric acid and hydroxybenzoic acid were elevated in PAO mice. These metabolites were significantly correlated with Bifidobacterium, Atomobium, Campylobacter, and Haemophilus, which are characteristic taxa in PAO mice. Conversely, health-associated oral microbiota were associated with higher levels of beneficial serum metabolites in HAO mice. The multi-omics approach used in this study revealed that periodontitis-associated oral microbiota is associated with the induction of disease phenotype when they colonized the gut of germ-free mice.

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Gut commensal Odoribacter splanchnicus alleviates hyperlipidemic periodontitis via the β-GPA-TLR4 axis

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