Exploration of Immunology

Table 2. Immunomodulatory effects of gut-derived SCFAs on periodontal immune responses.

Immune cell	Mechanism/receptor	SCFA effect	Periodontal outcomes	Key references
Macrophages	GPR43, GPR109A; HDAC inhibition	M2 polarization ↑; TNF-α, IL-6, IL-12 ↓; IL-10 ↑	Anti-inflammatory shift; reduced bone resorption	[12, 41]
Neutrophils	GPR43; NET regulation	Chemotaxis ↑; excessive NETosis ↓	Balanced pathogen control; limited tissue damage	[29, 49, 50]
Dendritic cells	GPR109A; HDAC inhibition	Tolerogenic phenotype; IL-12 ↓; Treg induction ↑	Reduced adaptive overactivation	[4, 29, 52, 53]
T cells (Treg/Th17)	HDAC inhibition; FOXP3 acetylation	Tregs ↑; Th17/Th1 ↓; IL-17, IFN-γ ↓	Restored immune tolerance	[4, 52]
Gingival fibroblasts	GPR41, GPR43; HDAC inhibition	IL-6, IL-8 ↓; collagen synthesis ↑; oxidative stress ↓	Enhanced tissue repair; reduced inflammatory signaling	[31, 44, 48]
Gingival epithelial cells	GPR43; barrier modulation; HDAC inhibition	Tight junction integrity ↑; pro-inflammatory cytokines ↓	Strengthened epithelial barrier; reduced microbial invasion	[30, 54, 55]

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Summary of the immunomodulatory effects of gut-derived SCFAs on periodontal immune responses, highlighting their role in promoting anti-inflammatory macrophage phenotypes and maintaining tissue homeostasis. SCFAs: short-chain fatty acids; HDAC: histone deacetylase; TNF-α: tumor necrosis factor-α; IL: interleukin; NET: neutrophil extracellular trap; Treg: regulatory T cell; FOXP3: forkhead box P3; IFN-γ: interferon-γ. ↑: upregulated; ↓: downregulated.

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DG: Conceptualization, Visualization, Writing—original draft, Writing—review & editing, Supervision. AY: Writing—original draft, Writing—review & editing. DP: Writing—original draft, Writing—review & editing. All authors read and approved the submitted version.

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The authors declare that they have no conflicts of interest.

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