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炎性小体与肠道稳态:调节并连接感染、炎症与微生物群

Inflammasomes and intestinal homeostasis: regulating and connecting infection, inflammation and the microbiota.

作者信息

Gagliani Nicola, Palm Noah W, de Zoete Marcel R, Flavell Richard A

机构信息

Department of Immunobiology, School of Medicine, Yale University, The Anlyan Center, 300 Cedar Street S560, S570 New Haven, CT 06519, USA.

Department of Immunobiology, School of Medicine, Yale University, The Anlyan Center, 300 Cedar Street S560, S570 New Haven, CT 06519, USA Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA.

出版信息

Int Immunol. 2014 Sep;26(9):495-9. doi: 10.1093/intimm/dxu066. Epub 2014 Jun 19.

DOI:10.1093/intimm/dxu066
PMID:24948595
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4200027/
Abstract

Inflammasomes are large cytosolic protein complexes that detect infection and stress-associated signals and promote immediate inflammatory responses. In the intestine, activation of the inflammasome leads to an inflammatory response that is important for controlling enteric infections but can also result in pathological tissue damage. Recent studies have suggested that the inflammasome also regulates intestinal homeostasis through its effects on the intestinal microbiota. Notably, many conflicting studies have been published regarding the effect of inflammasome deficiencies on intestinal homeostasis. Here, we attempt to reconcile these contrasting data by highlighting the many ways that the inflammasome contributes to intestinal homeostasis and pathology and exploring the potential role of alterations in the microbiota in these conflicting studies.

摘要

炎性小体是大型胞质蛋白复合物,可检测感染和应激相关信号并促进即时炎症反应。在肠道中,炎性小体的激活会引发炎症反应,这对于控制肠道感染很重要,但也可能导致病理性组织损伤。最近的研究表明,炎性小体还通过其对肠道微生物群的影响来调节肠道稳态。值得注意的是,关于炎性小体缺陷对肠道稳态的影响,已经发表了许多相互矛盾的研究。在这里,我们试图通过强调炎性小体促进肠道稳态和病理的多种方式,并探讨微生物群改变在这些相互矛盾的研究中的潜在作用,来调和这些相互矛盾的数据。

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本文引用的文献

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NLRP6 inflammasome orchestrates the colonic host-microbial interface by regulating goblet cell mucus secretion.NLRP6 炎性体通过调节杯状细胞黏液分泌来协调结肠的宿主-微生物界面。
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Inflammasome activation has an important role in the development of spontaneous colitis.炎性小体激活在自发性结肠炎的发展中起重要作用。
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Interactions between Nod-Like Receptors and Intestinal Bacteria.核苷酸结合寡聚化结构域样受体与肠道细菌之间的相互作用
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Nlrp3 activation in the intestinal epithelium protects against a mucosal pathogen.肠上皮细胞中 Nlrp3 的激活可预防黏膜病原体感染。
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NLRC4 expression in intestinal epithelial cells mediates protection against an enteric pathogen.肠上皮细胞中 NLRC4 的表达对肠道病原体起到保护作用。
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Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock.细胞质脂多糖激活半胱天冬酶-11:在 TLR4 非依赖性内毒素性休克中的意义。
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The Nlrp3 inflammasome regulates acute graft-versus-host disease.NLRP3 炎性小体调节急性移植物抗宿主病。
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Noncanonical inflammasome activation by intracellular LPS independent of TLR4.非经典炎性小体激活的细胞内 LPS 途径不依赖 TLR4。
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Microbiota-induced activation of epithelial IL-6 signaling links inflammasome-driven inflammation with transmissible cancer.微生物群诱导的上皮细胞白细胞介素 6 信号激活将炎性体驱动的炎症与可传播的癌症联系起来。
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Caspase-11 protects against bacteria that escape the vacuole.Caspase-11 可以保护细胞免受逃离溶酶体的细菌的侵害。
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