2017 Fiscal Year Final Research Report
The possibility that suppression of NETosis contributes to improvement of SLE
| Project/Area Number |
26461490
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
竹内 恵美子 北里大学, 医学部, 講師 (00406935)
大津 真 東京大学, 医科学研究所, 准教授 (30361330)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | 全身性エリテマトーデス / 好中球 / NETosis |
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| Outline of Final Research Achievements |
Neutrophils contribute to antimicrobial defense by releasing nuclear chromatin together with granule proteins to form an extra cellular mesh which binds and kills bacteria.This formation, called neutrophil extracellular traps (NETs), considered to be implicated in anti-nucleotide antibody (ANA) positive Systemic Lupus Erythematosus (SLE).Activated neutrophils has been shown to involve the NADPH oxidase (NOX2) mediated production of reactive oxygen species (ROS), leading to disintegration of the nuclear envelope and result in induction of NETosis. In this study, we investigated the causal relation between NOX2 dependent/independent ROS production and extracellular DNA releasing. It was observed that the deletion of NOX2 in neutrophils accelerated mitochondrial ROS production with lps stimulation and released oxidative damaged DNA. Addition of anti-oxDNA antibodies induced more NETosis in vitro assay. Therefore, further analysis of the pathogenesis of anti-oxDNA Ab is needed.
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| Free Research Field |
腎臓内科学
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