坏死性下垂
牙龈卟啉单胞菌
锡克
程序性细胞死亡
细胞生物学
炎症体
巨噬细胞
TLR2型
脂多糖
生物
细胞凋亡
信号转导
免疫学
炎症
TLR4型
酪氨酸激酶
体外
细菌
生物化学
遗传学
作者
Fei Geng,Junchao Liu,Chengcheng Yin,Shuwei Zhang,Yaping Pan,Hongchen Sun
标识
DOI:10.1080/20002297.2022.2041790
摘要
Necroptosis, a new type of regulated cell death with massive release of damage-associated molecular patterns (DAMPs), is involved in the pathogenesis of periodontitis. However, the role of necroptosis in oral epithelial cells and the following effect on macrophages activation remain unknown. Human immortalized oral epithelial cells were stimulated with Porphyromonas gingivalis lipopolysaccharide (LPS). Cell death was assessed while expressions of RIPK3/MLKL and toll-like receptors (TLRs) were evaluated. Necrosulfonamide (NSA), an inhibitor of MLKL was applied to block necroptosis. The expression of DAMPs and the epithelial connection protein were evaluated by qPCR and immunofluorescence, respectively. Immortalized human monocytes U937 were induced into the M0 or M2 subset, and influences of HIOECs-derived DAMPs on macrophage polarization as well as activation of the Mincle/SYK axis were assessed. P. gingivalis LPS could be recognized by TLR2 and regulates necroptosis of HIOECs by activating RIPK3/MLKL. NSA inhibited cell death of HIOECs, alleviated impaired epithelial connection, and inhibited expressions of DAMPs. Low dose of DAMPs derived from HIOECs promoted M2-like polarization by activating the Mincle/SYK axis, which was significantly suppressed with increased doses of DAMPs. P. gingivalis LPS destructed oral epithelial cells via RIPK3/MLKL-mediated necroptosis, which further regulated macrophage activation via DAMPs from oral epithelial cells.
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