『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=322120EID:322120, Map:0, LastModified:2017年6月28日(水) 11:32:17, Operator:[廣島 佑香], Avail:TRUE, Censor:0, Owner:[廣島 佑香], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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審査 (推奨): Peer Review [継承]
カテゴリ (推奨): 研究 [継承]
共著種別 (推奨): 徳島大学以外での単独著作 (徳島大学以外での単一の研究グループ(研究室等)内の研究 (単著も含む)) [継承]
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著者 (必須): 1.廣島 佑香 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔微生物学])
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2. (英) Hsu Kenneth (日) (読)
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3. (英) Tedla Nicodemus (日) (読)
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4. (英) Wong Wing Sze (日) (読)
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5. (英) Chow Sharron (日) (読)
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6. (英) Kawaguchi Naomi (日) (読)
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7. (英) Geczy L Carolyn (日) (読)
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題名 (必須): (英) S100A8/A9 and S100A9 reduce acute lung injury.  (日)    [継承]
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要約 (任意): (英) S100A8 and S100A9 are myeloid cell-derived proteins that are elevated in several types of inflammatory lung disorders. Pro- and anti-inflammatory properties are reported and these proteins are proposed to activate TLR4. S100A8 and S100A9 can function separately, likely through distinct receptors but a systematic comparison of their effects in vivo are limited. Here we assess inflammation in murine lung following S100A9 and S100A8/A9 inhalation. Unlike S100A8, S100A9 promoted mild neutrophil and lymphocyte influx, possibly mediated in part, by increased mast cell degranulation and selective upregulation of some chemokine genes, particularly CXCL-10. S100 proteins did not significantly induce proinflammatory mediators including TNF-, IL-1, IL-6 or serum amyloid A3 (SAA3). In contrast to S100A8, neither preparation induced S100A8 or IL-10 mRNA/protein in airway epithelial cells, or in tracheal epithelial cells in vitro. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung injury (ALI) provoked by LPS challenge but were somewhat less inhibitory, possibly because of differential effects on expression of some chemokines, IL-1, SAA3 and IL-10. Novel common pathways including increased induction of an NAD(+)-dependent protein deacetylase sirtuin-1 (SIRT1) that may reduce NF-B signalling, and increased STAT3 activation may reduce LPS activation. Results suggest a role for these proteins in normal homeostasis and protective mechanisms in the lung.Immunology and Cell Biology accepted article preview online, 11 January 2017. doi:10.1038/icb.2017.2.  (日)    [継承]
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誌名 (必須): Immunology and Cell Biology (Australian Society for Immunology)
(pISSN: 0818-9641, eISSN: 1440-1711)

ISSN (任意): 1440-1711
ISSN: 0818-9641 (pISSN: 0818-9641, eISSN: 1440-1711)
Title: Immunology and cell biology
Title(ISO): Immunol Cell Biol
Supplier: Australian and New Zealand Society for Immunology
Publisher: Wiley
 (NLM Catalog  (Wiley  (Scopus  (CrossRef (Scopus information is found. [need login])
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年月日 (必須): 西暦 2017年 1月 11日 (平成 29年 1月 11日) [継承]
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DOI (任意): 10.1038/icb.2017.2    (→Scopusで検索) [継承]
PMID (任意): 28074060    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Yuka Hiroshima, Kenneth Hsu, Nicodemus Tedla, Sze Wing Wong, Sharron Chow, Naomi Kawaguchi and Carolyn L Geczy : S100A8/A9 and S100A9 reduce acute lung injury., Immunology and Cell Biology, Vol.95, No.5, 461-472, 2017.
欧文冊子 ● Yuka Hiroshima, Kenneth Hsu, Nicodemus Tedla, Sze Wing Wong, Sharron Chow, Naomi Kawaguchi and Carolyn L Geczy : S100A8/A9 and S100A9 reduce acute lung injury., Immunology and Cell Biology, Vol.95, No.5, 461-472, 2017.

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