Upregulation of proteins of the NLRP3 inflammasome in patients with periodontitis and uncontrolled type 2 diabetes
Upregulation of proteins of the NLRP3 inflammasome in patients with periodontitis and uncontrolled type 2 diabetes
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DOI：
10.1111/odi.13003
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发表时间：
2019-03-01
期刊：
影响因子：
3.8
通讯作者：
Rubio-Infante, Nestor
中科院分区：
文献类型：
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作者：
Lilia Garcia-Hernandez, Ana;Enrique Munoz-Saavedra, Angel;Rubio-Infante, Nestor
目的研究慢性牙周炎（CP）和2型糖尿病（T2 D）患者牙周组织中NLRP 3炎性小体激活相关蛋白的表达，探讨糖尿病患者牙周组织病理过程的加重是否与NLRP 3炎性小体表达上调有关。材料和方法我们在三个研究组中进行了观察性、分析性、横断面研究：全身和口腔健康的个体，以及伴有和不伴有T2 D的CP患者。牙龈活检取自三个研究组。实时荧光定量PCR检测CASP 1、NLRP 3和ASC mRNA的表达，免疫组化检测NLRP 3和ASC蛋白的表达。使用ELISA测定龈沟液中IL-18和IL-1 β的定量。通过ANOVA分析结果，然后进行Tukey检验，以比较各组之间的差异。结果CP和未控制的T2 D患者存在严重的牙周病和炎症（PPD，p = 0.0072; CAL，p = 0.0480;骨丢失，p = 0.0088），CASP 1 mRNA表达水平较高（p = 0.0026），上皮和结缔组织中NLRP 3和ASC蛋白的染色模式更强，与健康或CP受试者相比，IL-18（p = 0.0063）和IL-1 β（p = 0.0018）的产生显著更高。结论牙周炎和未控制的T2 D患者中参与NLRP 3炎性体组分激活的基因和蛋白的上调提示在这些患者中观察到的导致牙周组织破坏的更严重的病理过程中可能起作用。
Objectives To evaluate the expression of proteins related to activation of the NLRP3 inflammasome in patients with chronic periodontitis (CP) and type 2 diabetes mellitus (T2D), and to determine whether the exacerbated periodontal pathological process observed in diabetic patients is related to its upregulation. Materials and Methods We performed an observational, analytical, cross-sectional study in three study groups: individuals systemically and orally healthy, and patients with CP with and without T2D. Gingival biopsies were taken from the three study groups. The expression of mRNAs for CASP1, NLRP3 and ASC was detected using real-time PCR, and the expression of NLRP3 and ASC proteins was determined by immunohistochemistry. The quantification of IL-18 and IL-1 beta was determined in the gingival crevicular fluid using ELISA. The results were analysed by ANOVA followed by Tukey's test to compare differences between individual groups. Results Patients with CP and uncontrolled T2D presented severe periodontal disease and inflammation (PPD, p = 0.0072; CAL, p = 0.0480; bone loss, p = 0.0088), higher levels of CASP1 mRNA expression (p = 0.0026), a stronger pattern of staining for NLRP3 and ASC proteins in the epithelium and connective tissues, and significantly higher production of IL-18 (p = 0.0063) and IL-1 beta (p = 0.0018) in comparison with healthy or CP subjects. Conclusion The upregulation of genes and proteins involved in the activation of the NLRP3 inflammasome components in patients with periodontitis and uncontrolled T2D suggests a possible role in the more severe pathological processes leading to destruction of periodontal tissues observed in these patients.