Hydrogen water alleviates obliterative airway disease in mice.


Journal

General thoracic and cardiovascular surgery
ISSN: 1863-6713
Titre abrégé: Gen Thorac Cardiovasc Surg
Pays: Japan
ID NLM: 101303952

Informations de publication

Date de publication:
Feb 2020
Historique:
received: 24 03 2019
accepted: 18 08 2019
pubmed: 31 8 2019
medline: 30 5 2020
entrez: 31 8 2019
Statut: ppublish

Résumé

Bronchiolitis obliterans syndrome arising from chronic airway inflammation is a leading cause of death following lung transplantation. Several studies have suggested that inhaled hydrogen can protect lung grafts from ischemia-reperfusion injury via anti-inflammatory and -oxidative mechanisms. We investigated whether molecular hydrogen-saturated water can preserve lung allograft function in a heterotopic tracheal allograft mouse model of obliterative airway disease METHODS: Obliterative airway disease was induced by heterotopically transplanting tracheal allografts from BALB/c donor mice into C57BL/6 recipient mice, which were subsequently administered hydrogen water (10 ppm) or tap water (control group) (n = 6 each) daily without any immunosuppressive treatment. Histological and immunohistochemical analyses were performed on days 7, 14, and 21. Hydrogen water decreased airway occlusion on day 14. No significant histological differences were observed on days 7 or 21. The cluster of differentiation 4/cluster of differentiation 3 ratio in tracheal allografts on day 14 was higher in the hydrogen water group than in control mice. Enzyme-linked immunosorbent assay performed on day 7 revealed that hydrogen water reduced the level of the pro-inflammatory cytokine interleukin-6 and increased that of forkhead box P3 transcription factor, suggesting an enhancement of regulatory T cell activity. Hydrogen water suppressed the development of mid-term obliterative airway disease in a mouse tracheal allograft model via anti-oxidant and -inflammatory mechanisms and through the activation of Tregs. Thus, hydrogen water is a potential treatment strategy for BOS that can improve the outcome of lung transplant patients.

Identifiants

pubmed: 31468277
doi: 10.1007/s11748-019-01195-3
pii: 10.1007/s11748-019-01195-3
doi:

Substances chimiques

Immunosuppressive Agents 0
Water 059QF0KO0R
Hydrogen 7YNJ3PO35Z

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

158-163

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Auteurs

Naoki Ozeki (N)

Department of Thoracic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan. naokiozeki@med.nagoya-u.ac.jp.

Aika Yamawaki-Ogata (A)

Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Yuji Narita (Y)

Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Shinji Mii (S)

Department of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Kaori Ushida (K)

Department of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Specimen Preparation Room for Optical Microscopic Examinations, Core Clinical Research Hospital Support Room, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Mikako Ito (M)

Division of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Shin-Ichi Hirano (SI)

MiZ Company Limited, Kamakura, Japan.

Ryosuke Kurokawa (R)

MiZ Company Limited, Kamakura, Japan.

Kinji Ohno (K)

Division of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Akihiko Usui (A)

Department of Cardiac Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

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Classifications MeSH