| Item type |
文献 / Documents(1) |
| 公開日 |
2020-03-17 |
| アクセス権 |
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アクセス権 |
open access |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 出版社版DOI |
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関連識別子 |
https://doi.org/10.1371/journal.pone.0205865 |
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関連名称 |
10.1371/journal.pone.0205865 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Host cellular unfolded protein response signaling regulates Campylobacter jejuni invasion |
| タイトル別表記 |
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その他のタイトル |
Functions of UPR in Campylobacter jejuni infection |
| 著者 |
テンタク, アヤ
下畑, 隆明
ハタヤマ, ショウ
キド, ジュンコ
Nguyen, Anh Quoc
カンダ, ユナ
フクシマ, シホ
上番増, 喬
イワタ, タケトシ
馬渡, 一諭
原田, 永勝
髙橋, 章
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| 抄録 |
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内容記述 |
Campylobacter jejuni is a major cause of bacterial foodborne illness in humans worldwide. Bacterial entry into a host eukaryotic cell involves the initial steps of adherence and invasion, which generally activate several cell-signaling pathways that induce the activation of innate defense systems, which leads to the release of proinflammatory cytokines and induction of apoptosis. Recent studies have reported that the unfolded protein response (UPR), a system to clear unfolded proteins from the endoplasmic reticulum (ER), also participates in the activation of cellular defense mechanisms in response to bacterial infection. However, no study has yet investigated the role of UPR in C. jejuni infection. Hence, the aim of this study was to deduce the role of UPR signaling via induction of ER stress in the process of C. jejuni infection. The results suggest that C. jejuni infection suppresses global protein translation. Also, 12 h of C. jejuni infection induced activation of the eIF2α pathway and expression of the transcription factor CHOP. Interestingly, bacterial invasion was facilitated by knockdown of UPR-associated signaling factors and treatment with the ER stress inducers, thapsigargin and tunicamycin, decreased the invasive ability of C. jejuni. An investigation into the mechanism of UPR-mediated inhibition of C. jejuni invasion showed that UPR signaling did not affect bacterial adhesion to or survival in the host cells. Further, Salmonella Enteritidis or FITC-dextran intake were not regulated by UPR signaling. These results indicated that the effect of UPR on intracellular intake was specifically found in C. jejuni infection. These findings are the first to describe the role of UPR in C. jejuni infection and revealed the participation of a new signaling pathway in C. jejuni invasion. UPR signaling is involved in defense against the early step of C. jejuni invasion and thus presents a potential therapeutic target for the treatment of C. jejuni infection. |
| 書誌情報 |
en : PLOS ONE
巻 13,
号 10,
p. e0205865,
発行日 2018-10-15
|
| 収録物ID |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
19326203 |
| 出版者 |
|
|
出版者 |
PLOS |
| 権利情報 |
|
|
権利情報 |
© 2018 Tentaku et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
| EID |
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|
識別子 |
351865 |
| 言語 |
|
|
言語 |
eng |
pone_13_10_e0205865.pdf (1.96 MB)
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