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Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity

High temperature and humidity (HTH) can cause diarrhea owing to food and drinking water contamination. However, their direct effects on gut microbiota and gastrointestinal inflammation are unknown. This study aimed to investigate the effects of HTH and probiotics on the microbiome. Twenty-one male m...

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Autores principales: Chen, Song, Zheng, Yuhua, Zhou, Yiqing, Guo, Weizhong, Tang, Qin, Rong, Guangli, Hu, Weiwei, Tang, Jianbang, Luo, Huanhuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904617/
https://www.ncbi.nlm.nih.gov/pubmed/31822775
http://dx.doi.org/10.1038/s41598-019-55337-x
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author Chen, Song
Zheng, Yuhua
Zhou, Yiqing
Guo, Weizhong
Tang, Qin
Rong, Guangli
Hu, Weiwei
Tang, Jianbang
Luo, Huanhuan
author_facet Chen, Song
Zheng, Yuhua
Zhou, Yiqing
Guo, Weizhong
Tang, Qin
Rong, Guangli
Hu, Weiwei
Tang, Jianbang
Luo, Huanhuan
author_sort Chen, Song
collection PubMed
description High temperature and humidity (HTH) can cause diarrhea owing to food and drinking water contamination. However, their direct effects on gut microbiota and gastrointestinal inflammation are unknown. This study aimed to investigate the effects of HTH and probiotics on the microbiome. Twenty-one male mice were randomly assigned to normal control (NC), HTH, and broad-spectrum probiotic-treated (PR) groups. HTH and PR groups were regularly housed at 30 ± 0.5 °C with humidity of 85–90% for eight consecutive weeks. A broad-spectrum probiotic was administrated to PR-group mice from day 50 to 56. Clinical signs were observed and gut microbiota were analyzed via 16 S rRNA-based functional metagenomics. Intestinal pathology and the expression of defensins and pro-inflammatory cytokines were also assessed. Mice in the HTH and PR groups gradually developed sticky or loose feces. The HTH group developed a distinct microbiota profile associated with augmented metabolism and human-like pathophysiologies upon suppression of environmental sensing. Pathological assays indicated minimal enteritis, increased bacterial translocation, and elevated intestinal pro-inflammatory cytokine levels. Thus, ambient HTH directly contributes to gut dysbiosis and minimal enteritis, whereas probiotics partially normalized the microbiota and ameliorated gut inflammation. This study provides novel insights into the pathogenesis of environment-associated diseases and offers a potential therapeutic approach.
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spelling pubmed-69046172019-12-13 Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity Chen, Song Zheng, Yuhua Zhou, Yiqing Guo, Weizhong Tang, Qin Rong, Guangli Hu, Weiwei Tang, Jianbang Luo, Huanhuan Sci Rep Article High temperature and humidity (HTH) can cause diarrhea owing to food and drinking water contamination. However, their direct effects on gut microbiota and gastrointestinal inflammation are unknown. This study aimed to investigate the effects of HTH and probiotics on the microbiome. Twenty-one male mice were randomly assigned to normal control (NC), HTH, and broad-spectrum probiotic-treated (PR) groups. HTH and PR groups were regularly housed at 30 ± 0.5 °C with humidity of 85–90% for eight consecutive weeks. A broad-spectrum probiotic was administrated to PR-group mice from day 50 to 56. Clinical signs were observed and gut microbiota were analyzed via 16 S rRNA-based functional metagenomics. Intestinal pathology and the expression of defensins and pro-inflammatory cytokines were also assessed. Mice in the HTH and PR groups gradually developed sticky or loose feces. The HTH group developed a distinct microbiota profile associated with augmented metabolism and human-like pathophysiologies upon suppression of environmental sensing. Pathological assays indicated minimal enteritis, increased bacterial translocation, and elevated intestinal pro-inflammatory cytokine levels. Thus, ambient HTH directly contributes to gut dysbiosis and minimal enteritis, whereas probiotics partially normalized the microbiota and ameliorated gut inflammation. This study provides novel insights into the pathogenesis of environment-associated diseases and offers a potential therapeutic approach. Nature Publishing Group UK 2019-12-10 /pmc/articles/PMC6904617/ /pubmed/31822775 http://dx.doi.org/10.1038/s41598-019-55337-x Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Chen, Song
Zheng, Yuhua
Zhou, Yiqing
Guo, Weizhong
Tang, Qin
Rong, Guangli
Hu, Weiwei
Tang, Jianbang
Luo, Huanhuan
Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity
title Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity
title_full Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity
title_fullStr Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity
title_full_unstemmed Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity
title_short Gut Dysbiosis with Minimal Enteritis Induced by High Temperature and Humidity
title_sort gut dysbiosis with minimal enteritis induced by high temperature and humidity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904617/
https://www.ncbi.nlm.nih.gov/pubmed/31822775
http://dx.doi.org/10.1038/s41598-019-55337-x
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