| Item type |
文献 / Documents(1) |
| 公開日 |
2021-02-08 |
| アクセス権 |
|
|
アクセス権 |
open access |
| 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 |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1038/icb.2017.2 |
|
|
言語 |
ja |
|
|
関連名称 |
10.1038/icb.2017.2 |
| 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 |
S100A8/A9 and S100A9 reduce acute lung injury |
|
言語 |
en |
| タイトル別表記 |
|
|
その他のタイトル |
Myeloid S100 proteins reduce lung inflammation |
|
言語 |
en |
| 著者 |
廣島, 佑香
Hsu, Kenneth
Tedla, Nicodemus
Wong, Sze Wing
Chow, Sharron
カワグチ, ナオミ
Geczy, Carolyn L
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
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‐α, interleukin‐1β (IL‐1β), 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 provoked by lipopolysaccharide (LPS) challenge but were somewhat less inhibitory, possibly because of differential effects on expression of some chemokines, IL‐1β, SAA3 and IL‐10. Novel common pathways including increased induction of an NAD+‐dependent protein deacetylase sirtuin‐1 that may reduce NF‐κB 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. |
|
言語 |
en |
| 書誌情報 |
en : Immunology & Cell Biology
巻 95,
号 5,
p. 461-472,
発行日 2017-01-31
|
| 収録物ID |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
14401711 |
| 収録物ID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA10678685 |
| 出版者 |
|
|
出版者 |
Australian and New Zealand Society for Immunology |
|
言語 |
en |
| 出版者 |
|
|
出版者 |
Wiley |
|
言語 |
en |
| 権利情報 |
|
|
言語 |
en |
|
権利情報 |
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission fromthe license holder to reproduce thematerial. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/ |
| EID |
|
|
識別子 |
322120 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
icb_95_5_461.pdf (2.99 MB)
.png)
