Detecting DNA: An Overview of DNA Recognition by Inflammasomes and Protection against Bacterial Respiratory Infections.
Detecting DNA: An Overview of DNA Recognition by Inflammasomes and Protection against Bacterial Respiratory Infections.
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作者：
先天免疫系统在细菌性疾病中调节宿主免疫防御中起关键作用。在感测病原体相关分子模式（PAMP）时，称为炎性体的多蛋白复合物通过促进病原体清除和细菌裂解而对细菌负荷起保护作用。这可以通过两种机制发生：（1）促炎细胞因子IL-1β/IL-18的裂解和（2）称为焦亡的炎性细胞死亡的启动。在最近的文献中，AIM 2样受体（ALR）和Nod样受体（NLR）炎性体激活已经涉及识别细菌DNA后的宿主保护。本文就细菌性呼吸道疾病中炎性小体识别DNA的机制作一综述。这一过程可以通过直接感应DNA或间接感应病原体相关的细胞内变化而发生。此外，DNA识别可以通过炎性小体-炎性小体相互作用来辅助，特别是NLRP 3的非典型炎性小体活化，以及与干扰素诱导型DNA传感器干扰素基因刺激因子（STING）和Z-DNA结合蛋白-1（ZBP 1）的串扰。最终，由炎性小体感测的细菌DNA在呼吸道疾病期间具有高度保护性，强调了炎性小体参与呼吸道的重要性。
The innate immune system plays a key role in modulating host immune defense during bacterial disease. Upon sensing pathogen-associated molecular patterns (PAMPs), the multi-protein complex known as the inflammasome serves a protective role against bacteria burden through facilitating pathogen clearance and bacteria lysis. This can occur through two mechanisms: (1) the cleavage of pro-inflammatory cytokines IL-1β/IL-18 and (2) the initiation of inflammatory cell death termed pyroptosis. In recent literature, AIM2-like Receptor (ALR) and Nod-like Receptor (NLR) inflammasome activation has been implicated in host protection following recognition of bacterial DNA. Here, we review current literature synthesizing mechanisms of DNA recognition by inflammasomes during bacterial respiratory disease. This process can occur through direct sensing of DNA or indirectly by sensing pathogen-associated intracellular changes. Additionally, DNA recognition may be assisted through inflammasome–inflammasome interactions, specifically non-canonical inflammasome activation of NLRP3, and crosstalk with the interferon-inducible DNA sensors Stimulator of Interferon Genes (STING) and Z-DNA Binding Protein-1 (ZBP1). Ultimately, bacterial DNA sensing by inflammasomes is highly protective during respiratory disease, emphasizing the importance of inflammasome involvement in the respiratory tract.
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DOI：
10.4049/jimmunol.1100381
发表时间：
2011-11-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Fang R;Tsuchiya K;Kawamura I;Shen Y;Hara H;Sakai S;Yamamoto T;Fernandes-Alnemri T;Yang R;Hernandez-Cuellar E;Dewamitta SR;Xu Y;Qu H;Alnemri ES;Mitsuyama M
通讯作者：
Mitsuyama M
影响因子：
6.4
作者：
Dilucca M;Ramos S;Shkarina K;Santos JC;Broz P
通讯作者：
Broz P
DOI：
10.4049/jimmunol.1502538
发表时间：
2016-04-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Corrales L;Woo SR;Williams JB;McWhirter SM;Dubensky TW Jr;Gajewski TF
通讯作者：
Gajewski TF
DOI：
10.1016/j.bbrc.2004.12.056
发表时间：
2005-02-18
影响因子：
3.1
作者：
Albrecht, M;Choubey, D;Lengauer, T
通讯作者：
Lengauer, T
影响因子：
6.7
作者：
Bast A;Krause K;Schmidt IH;Pudla M;Brakopp S;Hopf V;Breitbach K;Steinmetz I
通讯作者：
Steinmetz I