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Exploring the Mechanism of Oral Mucosal Immune Homeostasis Based on the IL-37 Signaling Pathway |
CHEN Yu1, DONG Weiwei1, ZHAO Yu2, JIN He1 |
1. Dental Department, Mingji Hospital Affiliated to Nanjing Medical University, NanJing 210000, China;
2. Department of Anesthesiology, Lu’an Shili Hospital, Lu’an 237000, China |
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Abstract Objective This study aims to elucidate the mechanism behind oral mucosal immune homeostasis by investigating the IL-37 signaling pathway. Methods An experimental model of oral inflammation was established in C57BL/6J mice through gingival nematode infection and induction of oral inflammation by human macrophages. The mice were categorized into control and rhIL-37b treatment groups. IL-37, inflammatory cytokines (IL-6, TNF-α, IL-10, IL-1β), and the NF-κB pathway were assessed using qPCR. Western blotting was employed to analyze the protein expression of IL-37 and the NF-κB pathway. Micro-computed tomography (microCT) imaging was utilized to quantify bone loss. Results Following gingival nematode infection, THP-1 cells exhibited elevated IL-37 mRNA expression. In human macrophages treated with rhIL-37b, production of IL-6, TNF-α, and IL-1β was reduced, accompanied by enhanced degradation of IκBα and diminished levels of phosphorylated p65 after gingival nematode infection, as compared to the control group. In the mouse periodontitis model, the rhIL-37b-treated group demonstrated a significant reduction in gingival inflammation and bone loss. Conclusion IL-37 plays a regulatory role in the inflammatory cytokine response of periodontitis by inhibiting the NF-κB signaling pathway. Consequently, IL-37 contributes to the mitigation of gingival tissue bone loss and cytokine expression.
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Received: 02 November 2022
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