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  1. H-1. がん進展制御研究所
  2. h-1 10. 学術雑誌掲載論文
  3. 1. 査読済論文

NLRP3 Mediates NF-κB activation and cytokine induction in microbially induced and sterile inflammation

https://doi.org/10.24517/00027505
https://doi.org/10.24517/00027505
6fd72cf6-a3bf-44fd-a6fe-d9cb8acf2092
名前 / ファイル ライセンス アクション
CA-PR-KINOSHITA-T-0119179.pdf CA-PR-KINOSHITA-T-0119179.pdf (1.5 MB)
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Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-05
タイトル
タイトル NLRP3 Mediates NF-κB activation and cytokine induction in microbially induced and sterile inflammation
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
ID登録
ID登録 10.24517/00027505
ID登録タイプ JaLC
著者 Kinoshita, Takeshi

× Kinoshita, Takeshi

WEKO 478
金沢大学研究者情報 20311681
研究者番号 20311681

Kinoshita, Takeshi

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Imamura, Ryu

× Imamura, Ryu

WEKO 256
e-Rad 10311680
金沢大学研究者情報 10311680
研究者番号 10311680

Imamura, Ryu

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Kushiyama, Hiroko

× Kushiyama, Hiroko

WEKO 47984

Kushiyama, Hiroko

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Suda, Takashi

× Suda, Takashi

WEKO 83
e-Rad 70250090
金沢大学研究者情報 70250090
研究者番号 70250090

Suda, Takashi

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著者別表示 木下, 健

× 木下, 健

木下, 健

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今村, 龍

× 今村, 龍

今村, 龍

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須田, 貴司

× 須田, 貴司

須田, 貴司

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書誌情報 PLoS ONE

巻 10, 号 3, p. e0119179, 発行日 2015-03-15
ISSN
収録物識別子タイプ ISSN
収録物識別子 1932-6203
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 10.1371/journal.pone.0119179
出版者
出版者 Public Library of Science
抄録
内容記述タイプ Abstract
内容記述 Nucleotide-binding domain and leucine-rich repeat-containing family, pyrin domain containing 3 (NLRP3) has recently emerged as a central regulator of innate immunity and inflammation in response to both sterile inflammatory and microbial invasion signals. Although its ability to drive proteolytic procaspase-1 processing has drawn more attention, NLPR3 can also activate NF-κ B. To clarify the physiological relevance of this latter function, we examined the effect of NLRP3 on NF-κB activation and cytokine induction in RNA-interferencebased NLRP3-knockdown cell lines generated from the human monocytic cell line THP-1. Knocking down NLRP3 reduced NF-κB activation and cytokine induction in the early stages of Staphylococcus aureus infection. Expression of cytokine genes induced by Staphylococcus aureus was not inhibited by a caspase-1 inhibitor, and did not occur through an autocrine mechanism in response to newly synthesized cytokines. We also demonstrated that NLRP3 could activate NF- κB and induce cytokines in response to sterile signals, monosodium urate crystals and aluminum adjuvant. Thus, NLRP3 mediates NF- κB activation in both sterile and microbially induced inflammation. Our findings show that not only does NLRP3 activate caspase-1 post-translationally, but it also induces multiple cytokine genes in the innate immune system.
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
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