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. 2025 Aug 8;16:1630828. doi: 10.3389/fmicb.2025.1630828

Figure 3.

Illustration showing the process of systemic inflammation initiated by the oral microbiome. This involves trained myelopoiesis in bone marrow and the STAT3 pathway, leading to hyperactive myeloid cells with NF-kB p65 nuclear translocation elevated, VCAM1 expression increased, and more adhesion to endothelial cells. At the same time, CAP+ monocytes extravasation increased. Inflammatory cytokines such as IL-6, TNF-?, and CRP are released, affecting adipose tissue. Adipokines secretion is altered, increasing leptin and resistin and decreasing adiponectin.

Impact of oral microbiome on systemic inflammation and adipokines secretion. The oral microbiome modulates the “central inflammation” hub function of bone marrow by altering its immune status, and influences systemic inflammation through cellular signaling pathways. Concurrently, inflammation itself regulates adipose tissue and affects adipokines secretion. Visual guide: Black arrows: Represent progressive relationships; Blue arrows: Show pathway modifications; Blue background: Highlights MetS mechanisms and phenotypes discussed in this study; Yellow background: Marks relevant signaling pathways; Green background: Shows adipokines secretion. Abbreviations: STAT3, signal transducers and activators of transcription 3; NF-κB nuclear factor-κB; VCAM 1, vascular cell adhesion molecule 1; CAP 1, caspase recruitment domain-containing protein 1; IL-6, interleukin-6; TNF-α, tumor necrosis factor-α; CRP, C-reactive protein. Created in BioRender. Yue, Z. (2025) https://BioRender.com/3m6ifm3.