PDF(Pubmed)
Abstract：
Inflammatory chemicals are released by the immune system in response to any perceived danger, including irritants and pathogenic organisms. The caspase activation and the response of inflammation are governed by inflammasomes, which are sensors and transmitters of the innate immune system. They have always been linked to swelling and pain. Research has mainly concentrated on the NOD-like protein transmitter 3 (NLRP3) inflammasome. Interleukin (IL)-1 and IL-18 are pro-inflammatory cytokines that are activated by the NOD-like antibody protein receptor 3 (NLRP3), which controls innate immune responses. The NLRP3 inflammasome has been associated with gum disease and other autoimmune inflammatory diseases in several studies. Scientists\' discovery of IL-1\'s central role in the pathophysiology of numerous autoimmune disorders has increased public awareness of these conditions. The first disease to be connected with aberrant inflammasome activation was the autoinflammatory cryopyrin-associated periodic syndrome (CAPS). Targeted therapeutics against IL-1 have been delayed in development because their underlying reasons are poorly understood. The NLRP3 inflammasome has recently been related to higher production and activation in periodontitis. Multiple periodontal cell types are controlled by the NLRP3 inflammasome. To promote osteoclast genesis, the NLRP3 inflammasome either increases receptor-activator of nuclear factor kappa beta ligand (RANKL) synthesis or decreases osteoclast-promoting gene (OPG) levels. By boosting cytokines that promote inflammation in the periodontal ligament fibroblasts and triggering apoptosis in osteoblasts, the NLRP3 inflammasome regulates immune cell activity. These findings support further investigation into the NLRP3 inflammasome as a therapeutic target for the medical treatment of periodontitis. This article provides a short overview of the NLRP3 inflammatory proteins and discusses their role in the onset of autoinflammatory disorders (AIDs) and periodontitis.
摘要：
免疫系统对任何感知到的危险都会释放出炎症化学物质，包括刺激物和致病生物。半胱天冬酶的激活和炎症反应是由炎性体控制的，它们是先天免疫系统的传感器和发射器。它们总是与肿胀和疼痛有关。研究主要集中在NOD样蛋白递质3（NLRP3）炎性体上。白细胞介素（IL）-1和IL-18是由NOD样抗体蛋白受体3（NLRP3）激活的促炎细胞因子，控制先天免疫反应。在一些研究中,NLRP3炎性体与牙龈疾病和其他自身免疫性炎性疾病相关。科学家发现IL-1在许多自身免疫性疾病的病理生理学中起着核心作用，提高了公众对这些疾病的认识。与异常炎性体激活有关的第一种疾病是自身炎性冷冻比林相关的周期性综合征（CAPS）。针对IL-1的靶向治疗剂在开发中被延迟,因为它们的潜在原因知之甚少。NLRP3炎性体最近与牙周炎中更高的产生和活化有关。多种牙周细胞类型受NLRP3炎性体控制。为了促进破骨细胞的发生，NLRP3炎性体增加核因子κβ受体激活剂配体(RANKL)合成或降低破骨细胞促进基因(OPG)水平.通过增强促进牙周膜成纤维细胞炎症并触发成骨细胞凋亡的细胞因子，NLRP3炎性体调节免疫细胞活性。这些发现支持对NLRP3炎性体作为牙周炎药物治疗的治疗靶标的进一步研究。本文简要概述了NLRP3炎性蛋白，并讨论了它们在自身炎症性疾病（AIDs）和牙周炎发作中的作用。
