ArticleMediators of inflammation2026
Signaling Through SCFA Receptors Gpr43 and Gpr109a Drives Pro-Inflammatory M1 Macrophage Polarization in Periodontitis.
Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Signaling Through SCFA Receptors Gpr43 and Gpr109a Drives Pro-Inflammatory M1 Macrophage Polarization in Periodontitis.Mediators of inflammation · 2026Article
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4 authors.
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Abstract
backgroundThis study investigated the link between an imbalance in microbiota-derived short-chain fatty acids (SCFAs) and dysregulated host immunity in periodontitis, focusing on the metabolic reprograming of inflammatory macrophages.
methodsWe conducted a systematic review and meta-analysis of SCFA levels. Bulk RNA sequencing (RNA-seq) data from human gingival tissue (n = 24) were analyzed for differential expression and pathway enrichment, with immune cell composition estimated by Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT). Mouse single-cell RNA-seq (scRNA-seq) data were integrated, and myeloid cells (MCs) were subset for detailed clustering, differential analysis, and pseudotime trajectory reconstruction.
resultsMeta-analysis indicated a decreasing, though nonsignificant, trend in butyrate levels in periodontitis. Bulk RNA-seq identified 692 differentially expressed genes (DEGs) enriched in immune and cytokine signaling pathways. Immune deconvolution revealed an increased proportion of M1 macrophages and Tregs, alongside a decrease in M2 macrophages. Single-cell analysis confirmed the significant expansion of M1-like macrophages, which highly expressed SCFA receptors (Gpr43 and Gpr109a), inflammatory transcription factors (Nfkb1 and Hif1a), and effector molecules (Il1b). The pseudotime trajectory demonstrated a continuous M2-to-M1 polarization, marked by a decline in M2 markers and a rise in M1 markers.
conclusionPeriodontitis is characterized by SCFA metabolic imbalance and a shift in MCs toward a pro-inflammatory M1 state. The upregulation of SCFA receptors and the NF-κB/HIF-1 axis in M1 macrophages suggests an "SCFA receptor-metabolic sensing-inflammatory transcription" mechanism drives disease progression, providing a rationale for therapeutic strategies targeting this pathway.
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