Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2013-05-29 |
タイトル |
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タイトル |
SHIP1 DELETION ENHANCES ROS PRODUCTION AND DECREASES SURVIVAL OF THE S. AUREUS INFECTED MICE |
言語 |
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言語 |
eng |
キーワード |
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主題Scheme |
Other |
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主題 |
Reactive oxygen species |
キーワード |
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主題Scheme |
Other |
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主題 |
NADPH oxidase |
キーワード |
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主題Scheme |
Other |
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主題 |
neutrophil |
キーワード |
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主題Scheme |
Other |
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主題 |
phospholipid |
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 |
著者 |
Chida, Shinsuke
Itoh, Reietsu
Kofuji, Satoshi
Eguchi, Satoshi
Takasuga, Shunsuke
Sasaki, Junko
Sasaki, Takehiko
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内容記述(抄録) |
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内容記述タイプ |
Other |
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内容記述 |
Reactive oxygen species (ROS) production by neutrophils is essential for host innate immune defense. However, although ROS production is advantageous for killing various infectious organisms, excessive ROS can cause tissue damage. Thus, ROS production by neutrophils must be tightly controlled. In this study, we investigated a role for SH2 domain-containing inositol- 5-phosphatase 1 (SHIP1), a PtdIns(3,4,5)P3 phosphatase, in ROS production by neutrophils using ship1−/− mice. SHIP1 deletion enhanced ROS production as well as the bacterial killing capability of neutrophils. However, the ship1−/− mice showed decreases survival of the mice infected with Staphylococcus aureus (S. aureus). Our results suggest that SHIP1 controls appropriate host defenses against S. aureus infections in mice. |
著者版フラグ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
書誌情報 |
秋田医学
巻 39,
号 3/4,
p. 95-101,
発行日 2013-03-30
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ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
03866106 |
NCID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AN00009294 |
出版者 |
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出版者 |
秋田医学会 |