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Possible Protective Role of NLRC4 Inflammasome in Periodontal Diseases: A Preliminary Study

机译:NLRC4炎症在牙周病中可能的保护作用:初步研究

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Introduction: Inflammasomes are multiprotein complexes, which regulate proinflammatory cytokines, Interleukin-18 (IL-18), and Interleukin-1β (IL-1β) that are associated with periodontal breakdown. This study investigated the expression of NOD-like receptor pyrin domain-containing-3 (NLRP3) and NOD-like receptor family CARD domain-containing protein 4 (NLRC4) inflammasomes in different periodontal diseases in humans and their potential association with IL-18 release in gingival crevicular fluid (GCF). Materials and Methods: A total of 45 participants (21 males and 24 females) divided into four groups; periodontally healthy (H), gingivitis (G), chronic periodontitis (CP), and aggressive periodontitis (AgP) based on periodontal examination. NLRC4 and NLRP3 expression were detected by immunohistochemistry in gingival tissue samples for all groups. Expression percentage (%) and staining intensity distribution score (SID) were calculated for both NLRC4 and NLRP3. IL-18 was measured in GCF via enzyme linked immunosorbent assay (ELISA). Results: Positive immunoreactivity was seen for NLRC4 and NLRP3 across groups. No differences were found for NLRC4 expression %, but SID scores were slightly higher in G and AgP compared to other groups (P 0.05). Results showed a significant increase of NRLP3 expression % in group CP compared to group H (P 0.05). IL-18 levels were significantly higher in AgP and CP groups compared to H and G groups (P 0.05). IL-18 significantly and positively correlated with clinical attachment levels across groups. Conclusion: Within the limitations of this preliminary study, we suggest that the NLRC4 platform may have a protective role contrary to the NLRP3 platform influencing IL-18 release and associated periodontal tissue breakdown.
机译:介绍:炎症是多律素复合物,其调节促炎细胞因子,白细胞介素-18(IL-18)和与牙周分解相关的白细胞介素-1β(IL-1β)。本研究研究了NOD样的受体吡林域域 - 3(NLRP3)和NOD样的受体家庭卡结构域的蛋白质4(NLRC4)炎症在人类的不同牙周病和与IL-18释放的潜在关联中在牙龈沟槽(GCF)中。材料和方法:共有45名参与者(21名男性和24名女性)分为四组;牙周健康(H),牙龈炎(G),慢性牙周炎(CP)和基于牙周检查的侵袭性牙周炎(AGP)。通过免疫组织化学在所有基团的牙龈组织样品中检测NLRC4和NLRP3表达。为NLRC4和NLRP3计算表达百分比(%)和染色强度分布得分(SID)。通过酶联免疫吸附试验(ELISA)在GCF中测量IL-18。结果:在群体中看到NLRC4和NLRP3的阳性免疫反应性。没有发现NLRC4表达%的差异,但与其他基团相比,G和AGP的SID分数略高(P&GT; 0.05)。结果表明,与H组(P 0.05)相比,CP组NRLP3表达%的显着增加(P 0.05)。与H和G基团相比,AGP和CP组IL-18水平显着高(P <0.05)。 IL-18与群体的临床附着水平显着和呈正相关。结论:在初步研究的局限内,我们建议NLRC4平台可能对影响IL-18释放的NLRP3平台和相关的牙周组织分解的保护作用。

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