Modulation of inflammasome activity by Porphyromonas gingivalis in periodontitis and associated systemic diseases.
Modulation of inflammasome activity by Porphyromonas gingivalis in periodontitis and associated systemic diseases.
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DOI：
10.3402/jom.v8.30385
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发表时间：
2016
影响因子：
4.5
通讯作者：
Yilmaz Ö
中科院分区：
文献类型：
--
作者：
Olsen I;Yilmaz Ö
炎性小体是位于细胞质中的大的多蛋白复合物。它们负责促炎细胞因子如白细胞介素-1 β（IL-1β）和IL-18的成熟以及炎症细胞死亡（所谓的焦亡）的激活。炎性小体响应于细胞感染、细胞应激或组织损伤而组装;促进炎症反应，并且在慢性炎症性疾病如牙周炎和几种慢性全身性疾病中调节先天免疫系统中非常重要。除了感知细胞的完整性，炎性小体还参与了原生微生物群和宿主之间的稳态互惠关系。有几种类型的炎性小体，其中NLRP 3在微生物发病机制中最具特征。许多机会性细菌试图逃避先天免疫系统，以便在宿主细胞中生存。其中之一是牙周病病原体牙龈卟啉单胞菌，其已被证明具有通过限制NLRP 3炎性体的活化来调节先天免疫的几种机制。其中，ATP-/P2 X7-信号通路不仅与牙周炎有关，而且与一些全身性疾病的发生有关。本文综述了牙龈卟啉单胞菌通过影响炎性小体活性来调节天然免疫的多种机制。
Inflammasomes are large multiprotein complexes localized in the cytoplasm of the cell. They are responsible for the maturation of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and IL-18 as well as for the activation of inflammatory cell death, the so-called pyroptosis. Inflammasomes assemble in response to cellular infection, cellular stress, or tissue damage; promote inflammatory responses and are of great importance in regulating the innate immune system in chronic inflammatory diseases such as periodontitis and several chronic systemic diseases. In addition to sensing cellular integrity, inflammasomes are involved in the homeostatic mutualism between the indigenous microbiota and the host. There are several types of inflammasomes of which NLRP3 is best characterized in microbial pathogenesis. Many opportunistic bacteria try to evade the innate immune system in order to survive in the host cells. One of these is the periodontopathogen Porphyromonas gingivalis which has been shown to have several mechanisms of modulating innate immunity by limiting the activation of the NLRP3 inflammasome. Among them, ATP-/P2X7- signaling is recently associated not only with periodontitis but also with development of several systemic diseases. The present paper reviews multiple mechanisms through which P. gingivalis can modify innate immunity by affecting inflammasome activity.