| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○招待 (推奨): |
| ○審査 (推奨): | □ | Peer Review
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| ○カテゴリ (推奨): | □ | 研究
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| ○共著種別 (推奨): | □ | 国内共著 (徳島大学内研究者と国内(学外)研究者との共同研究 (国外研究者を含まない))
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| ○学究種別 (推奨): | □ | 博士前期課程学生による研究報告
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| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Tentaku Aya (日) 天宅 あや (読) てんたく あや
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| ○学籍番号 (推奨): | □ | ****
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| 2. | 下畑 隆明
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| 3. | (英) Hatayama Sho (日) 畑山 翔 (読) はたやま しょう
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| ○学籍番号 (推奨): | □ | ****
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| 4. | (英) Kido Junko (日) 木戸 純子 (読) きど じゅんこ
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| ○学籍番号 (推奨): | □ | ****
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| 5. | (英) Nguyen Anh Quoc (日) Nguyen Anh Quoc (読) ぐえん くぉ あいん
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| ○学籍番号 (推奨): | □ | ****
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| 6. | (英) Kanda Yuna (日) 神田 結奈 (読) かんだ ゆうな
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| ○学籍番号 (推奨): | □ | ****
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| 7. | (英) Fukushima Shiho (日) 福島 志帆 (読) ふくしま しほ
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| ○学籍番号 (推奨): | □ | ****
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| 8. | 上番増 喬 ([徳島大学.大学院医歯薬学研究部.医学域.先端基礎栄養学教育研究プロジェクト]/[徳島大学.大学院医歯薬学研究部.医学域.栄養科学部門.医科栄養学系.予防環境栄養学])
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| 9. | (英) Iwata Taketoshi (日) (読)
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| 10. | 馬渡 一諭
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| 11. | 原田 永勝
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| 12. | 髙橋 章 ([徳島大学.大学院医歯薬学研究部.医学域.栄養科学部門.医科栄養学系.予防環境栄養学])
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| ○題名 (必須): | □ | (英) Host cellular unfolded protein response signaling regulates Campylobacter jejuni invasion. (日)
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| ○副題 (任意): |
| ○要約 (任意): | □ | (英) 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. (日)
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| ○キーワード (推奨): | 1. | (英) Caco-2 Cells (日) (読)
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| 2. | (英) Campylobacter jejuni (日) (読)
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| 3. | (英) Endoplasmic Reticulum Stress (日) (読)
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| 4. | (英) Thapsigargin (日) (読)
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| 5. | (英) Transcription Factor CHOP (日) (読)
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| 6. | (英) Tunicamycin (日) (読)
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| 7. | (英) Unfolded Protein Response (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | PLoS ONE (Public Library of Science)
(eISSN: 1932-6203)
| ○ISSN (任意): | □ | 1932-6203
ISSN: 1932-6203
(eISSN: 1932-6203) Title: PloS oneTitle(ISO): PLoS OnePublisher: PLOS (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 13
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| ○号 (必須): | □ | 10
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| ○頁 (必須): | □ |
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2018年 10月 15日 (平成 30年 10月 15日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1371/journal.pone.0205865 (→Scopusで検索)
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| ○PMID (任意): | □ | 30321237 (→Scopusで検索)
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| ○指導教員 (推奨): | 1. | 下畑 隆明
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| ○備考 (任意): | 1. | (英) PublicationType: Journal Article (日)
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| 2. | (英) PublicationType: Research Support, Non-U.S. Gov't (日)
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