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Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease

Kawasaki disease (KD) is a multi-systemic vasculitis of unknown etiology that occurs mainly in children, and the disturbance of gut microbiota is generally believed to cause a hyperimmune reaction triggering KD. The aim of the study was to investigate the alterations in the fecal microbiota and asse...

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Autores principales: Chen, Jie, Yue, Yanghua, Wang, Lu, Deng, Zhonghua, Yuan, Yonghua, Zhao, Menghua, Yuan, Zijie, Tan, Chaochao, Cao, Youde
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7471315/
https://www.ncbi.nlm.nih.gov/pubmed/32884012
http://dx.doi.org/10.1038/s41598-020-71371-6
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author Chen, Jie
Yue, Yanghua
Wang, Lu
Deng, Zhonghua
Yuan, Yonghua
Zhao, Menghua
Yuan, Zijie
Tan, Chaochao
Cao, Youde
author_facet Chen, Jie
Yue, Yanghua
Wang, Lu
Deng, Zhonghua
Yuan, Yonghua
Zhao, Menghua
Yuan, Zijie
Tan, Chaochao
Cao, Youde
author_sort Chen, Jie
collection PubMed
description Kawasaki disease (KD) is a multi-systemic vasculitis of unknown etiology that occurs mainly in children, and the disturbance of gut microbiota is generally believed to cause a hyperimmune reaction triggering KD. The aim of the study was to investigate the alterations in the fecal microbiota and assess its relationship with systemic inflammation. Totally 30 KD children were enrolled and followed up for 6 months, with another group of 30 age- and sex-matched healthy children as controls. Phylotype profiles of fecal microbial communities were analyzed using 16S rRNA gene sequencing. Serum inflammatory markers were detected by flow cytometer. We showed that KD children exhibited a significant reduction in fecal microbial diversity in the acute phase compared with the healthy controls. Enterococcus, Acinetobacter, Helicobacter, Lactococcus, Staphylococcus and Butyricimonas in acute KD children were significantly higher than the healthy children. Levels of systemic inflammation biomarkers, including IL-2, IL-4, IL-6, IL-10, TNF-α, and INF-γ, were significantly elevated in the acute KD children. Altered microbiota genera Enterococcus and Helicobacter abundances were shown to be correlated positively with IL-6, which were never previously reported in KD. This study suggested that gut microbiota alteration is closely associated with systemic inflammation, which provides a new perspective on the etiology and pathogenesis of KD.
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spelling pubmed-74713152020-09-04 Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease Chen, Jie Yue, Yanghua Wang, Lu Deng, Zhonghua Yuan, Yonghua Zhao, Menghua Yuan, Zijie Tan, Chaochao Cao, Youde Sci Rep Article Kawasaki disease (KD) is a multi-systemic vasculitis of unknown etiology that occurs mainly in children, and the disturbance of gut microbiota is generally believed to cause a hyperimmune reaction triggering KD. The aim of the study was to investigate the alterations in the fecal microbiota and assess its relationship with systemic inflammation. Totally 30 KD children were enrolled and followed up for 6 months, with another group of 30 age- and sex-matched healthy children as controls. Phylotype profiles of fecal microbial communities were analyzed using 16S rRNA gene sequencing. Serum inflammatory markers were detected by flow cytometer. We showed that KD children exhibited a significant reduction in fecal microbial diversity in the acute phase compared with the healthy controls. Enterococcus, Acinetobacter, Helicobacter, Lactococcus, Staphylococcus and Butyricimonas in acute KD children were significantly higher than the healthy children. Levels of systemic inflammation biomarkers, including IL-2, IL-4, IL-6, IL-10, TNF-α, and INF-γ, were significantly elevated in the acute KD children. Altered microbiota genera Enterococcus and Helicobacter abundances were shown to be correlated positively with IL-6, which were never previously reported in KD. This study suggested that gut microbiota alteration is closely associated with systemic inflammation, which provides a new perspective on the etiology and pathogenesis of KD. Nature Publishing Group UK 2020-09-03 /pmc/articles/PMC7471315/ /pubmed/32884012 http://dx.doi.org/10.1038/s41598-020-71371-6 Text en © The Author(s) 2020 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Chen, Jie
Yue, Yanghua
Wang, Lu
Deng, Zhonghua
Yuan, Yonghua
Zhao, Menghua
Yuan, Zijie
Tan, Chaochao
Cao, Youde
Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease
title Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease
title_full Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease
title_fullStr Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease
title_full_unstemmed Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease
title_short Altered gut microbiota correlated with systemic inflammation in children with Kawasaki disease
title_sort altered gut microbiota correlated with systemic inflammation in children with kawasaki disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7471315/
https://www.ncbi.nlm.nih.gov/pubmed/32884012
http://dx.doi.org/10.1038/s41598-020-71371-6
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