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Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice
BACKGROUND: Airway hyperresponsiveness (AHR) is one of the important traits that characterize bronchial asthma. Goishi tea is a post-heating fermented tea that has been reported to have higher free radical scavenging activity. In this study, we evaluated the prophylactic effects of Goishi tea on AHR...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3173379/ https://www.ncbi.nlm.nih.gov/pubmed/21831323 http://dx.doi.org/10.1186/1471-2172-12-45 |
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author | Hirota, Ryoji Ngatu, Nlandu R Miyamura, Mitsuhiko Nakamura, Hiroyuki Suganuma, Narufumi |
author_facet | Hirota, Ryoji Ngatu, Nlandu R Miyamura, Mitsuhiko Nakamura, Hiroyuki Suganuma, Narufumi |
author_sort | Hirota, Ryoji |
collection | PubMed |
description | BACKGROUND: Airway hyperresponsiveness (AHR) is one of the important traits that characterize bronchial asthma. Goishi tea is a post-heating fermented tea that has been reported to have higher free radical scavenging activity. In this study, we evaluated the prophylactic effects of Goishi tea on AHR in BALB/c mice. RESULTS: The number of inflammatory cells in BAL fluid was considerably reduced in Goishi tea/Der f and Gallic acid/Der f groups as compared with Tap water/Der f group. Regarding inflammatory cells in BAL, a significant reduction of eosinophils and neutrophils was observed in Goishi tea-treated mice (p < 0.01), as well as in the Gallic acid/Der f group (p < 0.05), as compared with Tap water/Der f group. In asthmatic mice (Tap water/Der f group), the intensity of airway resistance increased simultaneously with the increase in acetylcholine concentration in a dose-dependant way. AHR was significantly inhibited in Goishi tea/Der f and Gallic acid/Der f (p < 0.01) groups as compared with the Tap water/Der f group. Regarding serum specific-IgG(1), significantly lower levels of this antibody were observed in Goishi tea/Der f and Gallic acid/Der f groups as compared with the Tap water/Der f group (p < 0.05). In addition, adiponectin level was significantly higher in the Goishi tea group as compared with the Tap water treated mice (p < 0.01). CONCLUSIONS: The results suggest that Goishi tea consumption exerted an inhibitory effect on eosinophilic and neutrophilic infiltration in the lung, attenuated the increase in airway resistance and increased the production of adiponectin; thus reducing Der f induced allergic inflammatory process in mice. |
format | Online Article Text |
id | pubmed-3173379 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-31733792011-09-15 Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice Hirota, Ryoji Ngatu, Nlandu R Miyamura, Mitsuhiko Nakamura, Hiroyuki Suganuma, Narufumi BMC Immunol Research Article BACKGROUND: Airway hyperresponsiveness (AHR) is one of the important traits that characterize bronchial asthma. Goishi tea is a post-heating fermented tea that has been reported to have higher free radical scavenging activity. In this study, we evaluated the prophylactic effects of Goishi tea on AHR in BALB/c mice. RESULTS: The number of inflammatory cells in BAL fluid was considerably reduced in Goishi tea/Der f and Gallic acid/Der f groups as compared with Tap water/Der f group. Regarding inflammatory cells in BAL, a significant reduction of eosinophils and neutrophils was observed in Goishi tea-treated mice (p < 0.01), as well as in the Gallic acid/Der f group (p < 0.05), as compared with Tap water/Der f group. In asthmatic mice (Tap water/Der f group), the intensity of airway resistance increased simultaneously with the increase in acetylcholine concentration in a dose-dependant way. AHR was significantly inhibited in Goishi tea/Der f and Gallic acid/Der f (p < 0.01) groups as compared with the Tap water/Der f group. Regarding serum specific-IgG(1), significantly lower levels of this antibody were observed in Goishi tea/Der f and Gallic acid/Der f groups as compared with the Tap water/Der f group (p < 0.05). In addition, adiponectin level was significantly higher in the Goishi tea group as compared with the Tap water treated mice (p < 0.01). CONCLUSIONS: The results suggest that Goishi tea consumption exerted an inhibitory effect on eosinophilic and neutrophilic infiltration in the lung, attenuated the increase in airway resistance and increased the production of adiponectin; thus reducing Der f induced allergic inflammatory process in mice. BioMed Central 2011-08-11 /pmc/articles/PMC3173379/ /pubmed/21831323 http://dx.doi.org/10.1186/1471-2172-12-45 Text en Copyright ©2011 Hirota 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 Article Hirota, Ryoji Ngatu, Nlandu R Miyamura, Mitsuhiko Nakamura, Hiroyuki Suganuma, Narufumi Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice |
title | Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice |
title_full | Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice |
title_fullStr | Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice |
title_full_unstemmed | Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice |
title_short | Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice |
title_sort | goishi tea consumption inhibits airway hyperresponsiveness in balb/c mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3173379/ https://www.ncbi.nlm.nih.gov/pubmed/21831323 http://dx.doi.org/10.1186/1471-2172-12-45 |
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