Identification of organs of origin of macrophages that produce presepsin via neutrophil extracellulart trap phagocytosis 14 1
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DOI[10.50850/0002000064]to the data of the same series
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- Material Type
- 博士論文
- Volume
- 14 1
- Author/Editor
- Kondo, Akihiro
- Author Heading
- Publication Date
- 2024-07-1614 1
- Publication Date (W3CDTF)
- 2024-07-16
- Periodical title
- Scientific Reports
- Pages
- 16386-16386
- Degree Grantor
- 香川県立保健医療大学
- Date Granted
- 2025-03-09
- Date Granted (W3CDTF)
- 2025-03-09
- Dissertation Number
- 甲第8号
- Degree Type
- 博士(臨床検査学)
- Text Language Code
- eng
- Target Audience
- 一般
- Note (General)
- 出版タイプ: AM
- DOI
- 10.50850/0002000064
- Persistent ID (NDL)
- info:ndljp/pid/14627624
- Collection
- Collection (Materials For Handicapped People:1)
- Collection (particular)
- 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
- Acquisition Basis
- 博士論文(自動収集)
- Date Accepted (W3CDTF)
- 2026-02-07T09:27:52+09:00
- Format (IMT)
- application/pdf
- Access Restrictions
- 国立国会図書館内限定公開
- Service for the Digitized Contents Transmission Service
- 図書館・個人送信対象外
- Availability of remote photoduplication service
- 可
- Periodical Title (URI)
- Data Provider (Database)
- 国立国会図書館 : 国立国会図書館デジタルコレクション
- Summary, etc.
- Presepsin (P-SEP) is a specific biomarker for sepsis. Monocytes produce P-SEP by phagocytosing neutrophil extracellular traps (NETs). Herein, we investigated whether M1 macrophages (M1 MΦs) are the primary producers of P-SEP after NET phagocytosis. We co-cultured M1 MΦs and NETs from healthy participants, measured P-SEP levels in the culture medium supernatant, and detected P-SEP using western blotting. When NETs were co-cultured with M1 MΦs, the P-SEP level of the culture supernatant was high. Notably, we demonstrated, for the first time, the intracellular kinetics of P-SEP production by M1 MΦs via NET phagocytosis: M1 MΦs produced P-SEP intracellularly 15 min after NET phagocytosis and then released it extracellularly. In a sepsis mouse model, the blood NET ratio and P-SEP levels, detected using ELISA, were significantly increased (p < 0.0001). Intracellular P-SEP analysis via flow cytometry demonstrated that lung, liver, and kidney MΦs produced large amounts of P-SEP. Therefore, we identified these organs as the origin of M1 MΦs that produce P-SEP during sepsis. Our data indicate that the P-SEP level reflects the trend of NETs, suggesting that monitoring P-SEP can be used to both assess NET-induced organ damage in the lungs, liver, and kidneys during sepsis and determine treatment efficacy.
- DOI
- 10.50850/0002000064
- Format (IMT)
- application/pdf
- Source
- https://kagawa-puhs.repo.nii.ac.jp/record/2000064/files/222DS01博士論文本文.pdf (fulltext)
- Access Restrictions
- インターネット公開
- Data Provider (Database)
- 国立情報学研究所 : 学術機関リポジトリデータベース(IRDB)(機関リポジトリ)
- Original Data Provider (Database)
- 香川県立保健医療大学 : 香川県立保健医療大学リポジトリ