Exosomal microRNA‐155‐5p from PDLSCs regulated Th17/Treg balance by targeting sirtuin‐1 in chronic periodontitis

The mechanism of local inflammation and systemic injury in chronic periodontitis is complicated, in which and exosomes play an important role. In our study, we found that T helper cell 17 (Th17)/regulatory T cell (Treg) balance is destabilized in the peripheral blood of patients with periodontitis, with upregulated Th17 or downregulated Treg, respectively. Porphyromonas gingivalis lipopolysaccharide (LPS) was used to simulate the inflammatory microenvironment of chronic periodontitis. The exosomes were extracted from periodontal ligament stem cells (PDLSCs) in LPS‐induced periodontitis environment, which inversely effected on CD4+ T cells under normal and inflammatory conditions. Furthermore, compared with exosomes from normal PDLSCs, lower expression of microRNA‐155‐5p (miR‐155‐5p) and higher expression of Sirtuin‐1 (SIRT1) were observed in exosomes from LPS‐stimulated PDLSCs. Exosomes from PDLSCs alleviated inflammatory microenvironment through Th17/Treg/miR‐155‐5p/SIRT1 regulatory network. This study aimed to find the “switching” factors that affected the further deterioration of periodontitis to maximally control the multiple downstream damage signal factors to further understand periodontitis and find new targets for its treatment. The mechanism of how exosomes from periodontal ligament stem cells (PDLSCs) alleviated inflammatory microenvironment through T helper cell 17 (Th17)/regulatory T cell (Treg)/microRNA‐155‐5p (miR‐155‐5p)/Sirtuin‐1 (SIRT1) regulatory network. PDLSCs in the normal environment was favorable for the maintenance of Th17/Treg balance. The expression of miR‐155‐5p is decreased in exosomes released by PDLSCs in the inflammatory microenvironment. After ingestion by CD4+ T cells, the expression of SIRT1 in CD4+ T cells is increased, causing the upregulation of Th17 and the downregulation of Treg.