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Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study

BACKGROUND: Extracellular adenosine 5'-triphosphate (ATP) is an endogenous signaling molecule involved in multiple biological phenomena, including inflammation. The effects of extracellular ATP in the lung have not been fully clarified. This study examined 1) the biological roles of extracellul...

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Autores principales: Matsuyama, Hiroki, Amaya, Fumimasa, Hashimoto, Soshi, Ueno, Hiroshi, Beppu, Satoru, Mizuta, Mitsuhiko, Shime, Nobuaki, Ishizaka, Akitoshi, Hashimoto, Satoru
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627837/
https://www.ncbi.nlm.nih.gov/pubmed/19077288
http://dx.doi.org/10.1186/1465-9921-9-79
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author Matsuyama, Hiroki
Amaya, Fumimasa
Hashimoto, Soshi
Ueno, Hiroshi
Beppu, Satoru
Mizuta, Mitsuhiko
Shime, Nobuaki
Ishizaka, Akitoshi
Hashimoto, Satoru
author_facet Matsuyama, Hiroki
Amaya, Fumimasa
Hashimoto, Soshi
Ueno, Hiroshi
Beppu, Satoru
Mizuta, Mitsuhiko
Shime, Nobuaki
Ishizaka, Akitoshi
Hashimoto, Satoru
author_sort Matsuyama, Hiroki
collection PubMed
description BACKGROUND: Extracellular adenosine 5'-triphosphate (ATP) is an endogenous signaling molecule involved in multiple biological phenomena, including inflammation. The effects of extracellular ATP in the lung have not been fully clarified. This study examined 1) the biological roles of extracellular ATP in the pathogenesis of lung inflammation and 2) the possibility of involvement of extracellular ATP in mechanical ventilation-induced lung injury. METHODS: The effects of intratracheal ATP on lung permeability, edema or lung inflammation were assessed by measurements of the lung wet-to-dry weight ratio and lung permeability index, immunohistochemistry and expression of key cytokines by real-time polymerase chain reaction. The ATP concentration in broncho-alveolar lavage (BAL) fluid from mice mechanically ventilated was measured by luciferin-luciferase assay. The suppressive effects of a P2 receptor antagonist on ventilator-induced lung inflammation were also examined. RESULTS: ATP induced inflammatory reactions in the lung mainly via the ATP-P2Y receptor system. These reactions were alleviated by the co-administration of a specific P2 receptor antagonist. Mechanical ventilation with a large tidal volume caused lung inflammation and increased the ATP concentration in BAL fluid. P2 receptor antagonism partially mitigated the inflammatory effects of large tidal volume ventilation. CONCLUSION: Our observations suggest that the ATP-P2Y receptor system is partially involved in the pathogenesis of ventilator-induced lung injury.
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spelling pubmed-26278372009-01-17 Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study Matsuyama, Hiroki Amaya, Fumimasa Hashimoto, Soshi Ueno, Hiroshi Beppu, Satoru Mizuta, Mitsuhiko Shime, Nobuaki Ishizaka, Akitoshi Hashimoto, Satoru Respir Res Research BACKGROUND: Extracellular adenosine 5'-triphosphate (ATP) is an endogenous signaling molecule involved in multiple biological phenomena, including inflammation. The effects of extracellular ATP in the lung have not been fully clarified. This study examined 1) the biological roles of extracellular ATP in the pathogenesis of lung inflammation and 2) the possibility of involvement of extracellular ATP in mechanical ventilation-induced lung injury. METHODS: The effects of intratracheal ATP on lung permeability, edema or lung inflammation were assessed by measurements of the lung wet-to-dry weight ratio and lung permeability index, immunohistochemistry and expression of key cytokines by real-time polymerase chain reaction. The ATP concentration in broncho-alveolar lavage (BAL) fluid from mice mechanically ventilated was measured by luciferin-luciferase assay. The suppressive effects of a P2 receptor antagonist on ventilator-induced lung inflammation were also examined. RESULTS: ATP induced inflammatory reactions in the lung mainly via the ATP-P2Y receptor system. These reactions were alleviated by the co-administration of a specific P2 receptor antagonist. Mechanical ventilation with a large tidal volume caused lung inflammation and increased the ATP concentration in BAL fluid. P2 receptor antagonism partially mitigated the inflammatory effects of large tidal volume ventilation. CONCLUSION: Our observations suggest that the ATP-P2Y receptor system is partially involved in the pathogenesis of ventilator-induced lung injury. BioMed Central 2008 2008-12-13 /pmc/articles/PMC2627837/ /pubmed/19077288 http://dx.doi.org/10.1186/1465-9921-9-79 Text en Copyright © 2008 Matsuyama et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Matsuyama, Hiroki
Amaya, Fumimasa
Hashimoto, Soshi
Ueno, Hiroshi
Beppu, Satoru
Mizuta, Mitsuhiko
Shime, Nobuaki
Ishizaka, Akitoshi
Hashimoto, Satoru
Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study
title Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study
title_full Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study
title_fullStr Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study
title_full_unstemmed Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study
title_short Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study
title_sort acute lung inflammation and ventilator-induced lung injury caused by atp via the p2y receptors: an experimental study
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627837/
https://www.ncbi.nlm.nih.gov/pubmed/19077288
http://dx.doi.org/10.1186/1465-9921-9-79
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