Dental Calculus Stimulates Interleukin-1β Secretion by Activating NLRP3 Inflammasome in Human and Mouse Phagocytes.
Dental Calculus Stimulates Interleukin-1β Secretion by Activating NLRP3 Inflammasome in Human and Mouse Phagocytes.
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DOI：
10.1371/journal.pone.0162865
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Hara Y
中科院分区：
文献类型：
--
作者：
Montenegro Raudales JL;Yoshimura A;Sm Z;Kaneko T;Ozaki Y;Ukai T;Miyazaki T;Latz E;Hara Y
牙结石是一种与牙周炎有关的矿化存款。牙结石中含有的细菌成分可以被宿主免疫传感器（例如Toll样受体（TLR））识别，并诱导促炎细胞因子（例如IL-1β）的转录。研究表明，结晶颗粒的细胞摄取可触发NLRP 3炎性小体活化，导致IL-1β前体裂解成其成熟形式。牙周袋中牙结石的吞噬作用可能导致IL-1β的分泌，促进牙周组织的炎症反应。然而，尚未研究牙结石诱导人吞噬细胞分泌IL-1β的能力。为了研究这一点，我们用牙周炎患者的牙结石刺激人多形核白细胞（PMNs）和外周血单个核细胞（PBMCs），并用ELISA法测定IL-1β的分泌。我们发现结石诱导人PMN和PBMC分泌IL-1β。结石还在野生型小鼠的巨噬细胞中诱导IL-1β，但在NLRP 3和ASC缺陷小鼠的巨噬细胞中不诱导，表明NLRP 3和ASC参与其中。多粘菌素B可抑制IL-1β的诱导，提示LPS是结石中诱导IL-1β前体转录的成分之一。为了分析无机结构的影响，我们在250°C下烘烤结石1小时。这种烘烤的结石未能诱导pro-IL-1β转录。然而，它确实在脂质A致敏的细胞中诱导IL-1β分泌，表明结石的晶体结构诱导炎性小体活化。此外，羟基磷灰石晶体，牙结石的一种成分，诱导小鼠巨噬细胞中的IL-1β，和烤结石诱导的IL-1β在脂质A致敏的人PMN和PBMC中。这些结果表明，牙结石通过人和小鼠吞噬细胞中的NLRP 3炎性体刺激IL-1β分泌，并且晶体结构在NLRP 3炎性体的活化中具有部分作用。
Dental calculus is a mineralized deposit associated with periodontitis. The bacterial components contained in dental calculus can be recognized by host immune sensors, such as Toll-like receptors (TLRs), and induce transcription of proinflammatory cytokines, such as IL-1β. Studies have shown that cellular uptake of crystalline particles may trigger NLRP3 inflammasome activation, leading to the cleavage of the IL-1β precursor to its mature form. Phagocytosis of dental calculus in the periodontal pocket may therefore lead to the secretion of IL-1β, promoting inflammatory responses in periodontal tissues. However, the capacity of dental calculus to induce IL-1β secretion in human phagocytes has not been explored. To study this, we stimulated human polymorphonuclear leukocytes (PMNs) and peripheral blood mononuclear cells (PBMCs) with dental calculus collected from periodontitis patients, and measured IL-1β secretion by ELISA. We found that calculus induced IL-1β secretion in both human PMNs and PBMCs. Calculus also induced IL-1β in macrophages from wild-type mice, but not in macrophages from NLRP3- and ASC-deficient mice, indicating the involvement of NLRP3 and ASC. IL-1β induction was inhibited by polymyxin B, suggesting that LPS is one of the components of calculus that induces pro-IL-1β transcription. To analyze the effect of the inorganic structure, we baked calculus at 250°C for 1 h. This baked calculus failed to induce pro-IL-1β transcription. However, it did induce IL-1β secretion in lipid A-primed cells, indicating that the crystalline structure of calculus induces inflammasome activation. Furthermore, hydroxyapatite crystals, a component of dental calculus, induced IL-1β in mouse macrophages, and baked calculus induced IL-1β in lipid A-primed human PMNs and PBMCs. These results indicate that dental calculus stimulates IL-1β secretion via NLRP3 inflammasome in human and mouse phagocytes, and that the crystalline structure has a partial role in the activation of NLRP3 inflammasome.
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影响因子：
8.7
作者：
Horvath GL;Schrum JE;De Nardo CM;Latz E
通讯作者：
Latz E
影响因子：
64.8
作者：
GOWEN, M;WOOD, DD;RUSSELL, RGG
通讯作者：
RUSSELL, RGG
影响因子：
30.5
作者：
通讯作者：
--
DOI：
10.4049/jimmunol.1202737
发表时间：
2013-01-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
He Y;Franchi L;Núñez G
通讯作者：
Núñez G
高血糖导致牙周炎：NLRP3 通路通过参与口腔牙龈上皮的先天免疫而参与其中
影响因子：
4.3
作者：
Huang, Xin;Yang, Xi;Zhang, Jincai
通讯作者：
Zhang, Jincai