ID | 114338 |
タイトル別表記 | Functions of UPR in Campylobacter jejuni infection
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著者 |
Tentaku, Aya
Tokushima University
Hatayama, Sho
Tokushima University
Kido, Junko
Tokushima University
Nguyen, Anh Quoc
Tokushima University
Kanda, Yuna
Tokushima University
Fukushima, Shiho
Tokushima University
Iwata, Taketoshi
National Agriculture and Food Research Organization
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資料タイプ |
学術雑誌論文
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抄録 | 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.
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掲載誌名 |
PLOS ONE
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ISSN | 19326203
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出版者 | PLOS
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巻 | 13
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号 | 10
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開始ページ | e0205865
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発行日 | 2018-10-15
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権利情報 | © 2018 Tentaku et al. This is an open access article distributed under the terms of the Creative Commons Attribution License( https://creativecommons.org/licenses/by/4.0/ ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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言語 |
eng
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出版社版
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部局 |
医学系
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