Inflammasomes as contributors to periodontal disease.
Inflammasomes as contributors to periodontal disease.
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DOI：
10.1002/jper.20-0157
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发表时间：
2020-10
影响因子：
4.3
通讯作者：
Marchesan JT
中科院分区：
文献类型：
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作者：
Marchesan JT
一项对250万个标记物进行的全基因组关联研究确定了独特的生物学信息牙周复合体特征，具有不同的微生物群落和白细胞介素-1 β（IL-1β）水平。每个性状与不同的单核苷酸多态性相关。这些变体包括与免疫应答、微生物定植和上皮屏障功能相关的基因。特定的一组变异导致个体的生物学路径，这些生物学路径汇聚成牙周组织破坏的重叠临床表型。这一概念表明牙周病是一组不同的条件。我们确定了炎症体基因干扰素γ诱导蛋白16（IFI 16）和黑色素瘤2（AIM 2）中缺失的多态性，这些基因与牙周病的严重程度增加相关。炎性小体对病原体或组织“危险”信号作出反应，并组装成多蛋白“机器”，这对于将促炎介质IL-1β裂解成活性形式至关重要。因此，了解IFI 16和AIM 2的变体如何有助于牙周病的发病机制，可能会导致针对个体生物学变异和口腔健康的精确治疗的治疗选择。
A genome‐wide association study of ≈2.5 million markers identified unique biologically informed periodontal complex traits with distinct microbial communities and interleukin‐1β (IL‐1β) levels. Each trait was associated with different single nucleotide polymorphisms. These variants include genes associated with immune responses, microbial colonization, and the epithelial barrier function. The specific set of variants leads to individual biological paths that converge into an overlapping clinical phenotype of periodontal tissue destruction. This concept suggests that periodontal disease is a group of distinct conditions. We identified polymorphisms in inflammasome genes interferon gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) that were associated with increased severity of periodontal disease. Inflammasomes respond to pathogen or tissue “danger” signals and assemble into multiprotein “machineries” that are essential for the cleavage of proinflammatory mediator IL‐1β into an active form. Thus, understanding how variants of IFI16 and AIM2 contribute to periodontal disease pathogenesis may lead to treatment options that address individual biological variations and precision therapies for oral health.