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TLR2 和 NLRP3 炎性小体介导 - 感染树突状细胞中的 IL-1β 产生。

TLR2 and the NLRP3 inflammasome mediate IL-1β production in -infected dendritic cells.

机构信息

Laboratory Animal Medicine, College of Veterinary Medicine and BK 21 PLUS Project Team, Chonnam National University, Gwangju, Republic of Korea.

Department of Oral Pathology, School of Dentistry, Institute of Biodegradable material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Republic of Korea.

出版信息

Int J Med Sci. 2021 Jan 1;18(2):432-440. doi: 10.7150/ijms.47197. eCollection 2021.

DOI:10.7150/ijms.47197
PMID:33390812
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7757152/
Abstract

is an oral pathogen that is frequently observed in the subgingival plaque of periodontitis patients. Interleukin-1β (IL-1β) is known to be involved in the immunopathology of periodontal diseases and has been implicated in the destruction of bone. In this study, we investigated the mechanism of IL-1β production by in murine bone marrow-derived dendritic cells (BMDCs). Our results showed that a host receptor, Toll-like receptor 2 (TLR2), but not TLR4 is required for pro-IL-1β induction and nucleotide-binding oligomerization domain like receptor pyrin domain containing 3 (NLRP3) priming in BMDCs in response to and activation of the NLRP3 inflammasome is necessary for processing of pro-IL-1β into mature IL-1β. In addition, an inhibitor assay revealed that production of reactive oxygen species, P2XR activity, and release of cathepsin B are involved in IL-1β production in BMDCs in response to

摘要

牙龈卟啉单胞菌是一种常见于牙周炎患者龈下菌斑中的口腔病原体。白细胞介素-1β(IL-1β)已知参与牙周病的免疫病理学,并与骨破坏有关。在这项研究中,我们研究了牙龈卟啉单胞菌在小鼠骨髓来源树突状细胞(BMDCs)中产生 IL-1β 的机制。我们的结果表明,宿主受体 Toll 样受体 2(TLR2),而不是 TLR4,是诱导 BMDCs 中前 IL-1β诱导和核苷酸结合寡聚结构域样受体含吡咯烷结构域 3(NLRP3)引发所必需的,对 NLRP3 炎性小体的激活对于将前 IL-1β加工成熟为 IL-1β是必要的。此外,抑制剂测定表明,在 BMDCs 中,活性氧物质的产生、P2XR 活性和组织蛋白酶 B 的释放参与了对 的反应中 IL-1β 的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/68c5ed39d4b3/ijmsv18p0432g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/fbde62b3614e/ijmsv18p0432g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/dcb9b78b4a27/ijmsv18p0432g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/fa1178129141/ijmsv18p0432g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/a4b104c8a15c/ijmsv18p0432g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/68c5ed39d4b3/ijmsv18p0432g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/fbde62b3614e/ijmsv18p0432g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/5e8f017e90fa/ijmsv18p0432g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/dcb9b78b4a27/ijmsv18p0432g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/fa1178129141/ijmsv18p0432g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90b3/7757152/68c5ed39d4b3/ijmsv18p0432g006.jpg

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