ID | 62859 |
フルテキストURL | |
著者 |
Aokage, Toshiyuki
Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Seya, Mizuki
Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Hirayama, Takahiro
Department of Disaster Medicine and Management, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Nojima, Tsuyoshi
Department of Primary Care and Medical Education, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
ORCID
Kaken ID
publons
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Iketani, Masumi
Department of Biological Process of Aging, Tokyo Metropolitan Institute of Gerontology
Ishikawa, Michiko
Department of Emergency, Disaster and Critical Care Medicine, Hyogo College of Medicine
Terasaki, Yasuhiro
Department of Analytic Human Pathology, Nippon Medical School
Taniguchi, Akihiko
Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kaken ID
Miyahara, Nobuaki
Department of Medical Technology, Okayama University Graduate School of Health Sciences
Kaken ID
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Nakao, Atsunori
Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kaken ID
Ohsawa, Ikuroh
Department of Biological Process of Aging, Tokyo Metropolitan Institute of Gerontology
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抄録 | Background : Acute respiratory distress syndrome, which is caused by acute lung injury, is a destructive respiratory disorder caused by a systemic inflammatory response. Persistent inflammation results in irreversible alveolar fibrosis. Because hydrogen gas possesses anti-inflammatory properties, we hypothesized that daily repeated inhalation of hydrogen gas could suppress persistent lung inflammation by inducing functional changes in macrophages, and consequently inhibit lung fibrosis during late-phase lung injury.
Methods : To test this hypothesis, lung injury was induced in mice by intratracheal administration of bleomycin (1.0 mg/kg). Mice were exposed to control gas (air) or hydrogen (3.2% in air) for 6 h every day for 7 or 21 days. Respiratory physiology, tissue pathology, markers of inflammation, and macrophage phenotypes were examined. Results : Mice with bleomycin-induced lung injury that received daily hydrogen therapy for 21 days (BH group) exhibited higher static compliance (0.056 mL/cmH(2)O, 95% CI 0.047-0.064) than mice with bleomycin-induced lung injury exposed only to air (BA group; 0.042 mL/cmH(2)O, 95% CI 0.031-0.053, p = 0.02) and lower static elastance (BH 18.8 cmH(2)O/mL, [95% CI 15.4-22.2] vs. BA 26.7 cmH(2)O/mL [95% CI 19.6-33.8], p = 0.02). When the mRNA levels of pro-inflammatory cytokines were examined 7 days after bleomycin administration, interleukin (IL)-6, IL-4 and IL-13 were significantly lower in the BH group than in the BA group. There were significantly fewer M2-biased macrophages in the alveolar interstitium of the BH group than in the BA group (3.1% [95% CI 1.6-4.5%] vs. 1.1% [95% CI 0.3-1.8%], p = 0.008). Conclusions The results suggest that hydrogen inhalation inhibits the deterioration of respiratory physiological function and alveolar fibrosis in this model of lung injury. |
キーワード | Acute respiratory distress syndrome
Bleomycin-induced lung injury
Macrophage
Molecular hydrogen
Lung fibrosis
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発行日 | 2021-10-31
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出版物タイトル |
BMC Pulmonary Medicine
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巻 | 21巻
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号 | 1号
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出版者 | BMC
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開始ページ | 339
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ISSN | 1471-2466
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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著作権者 | © The Author(s) 2021.
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.1186/s12890-021-01712-2
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ライセンス | http://creativecommons.org/licenses/by/4.0/
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助成機関名 |
Ministry of Education, Culture, Sports, Science and Technology
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助成番号 | 19K09416
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