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Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients
BACKGROUND: Psoriasis is an inflammatory skin disease associated with multiple comorbidities and substantially diminishes patients’ quality of life. The gut microbiome has become a hot topic in psoriasis as it has been shown to affect both allergy and autoimmunity diseases in recent studies. Our obj...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7941898/ https://www.ncbi.nlm.nih.gov/pubmed/33685393 http://dx.doi.org/10.1186/s12866-021-02125-1 |
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author | Zhang, Xinyue Shi, Linjing Sun, Ting Guo, Kun Geng, Songmei |
author_facet | Zhang, Xinyue Shi, Linjing Sun, Ting Guo, Kun Geng, Songmei |
author_sort | Zhang, Xinyue |
collection | PubMed |
description | BACKGROUND: Psoriasis is an inflammatory skin disease associated with multiple comorbidities and substantially diminishes patients’ quality of life. The gut microbiome has become a hot topic in psoriasis as it has been shown to affect both allergy and autoimmunity diseases in recent studies. Our objective was to identify differences in the fecal microbial composition of patients with psoriasis compared with healthy individuals to unravel the microbiota profiling in this autoimmune disease. RESULTS: We collected fecal samples from 30 psoriasis patients and 30 healthy controls, sequenced them by 16S rRNA high-throughput sequencing, and identified the gut microbial composition using bioinformatic analyses including Quantitative Insights into Microbial Ecology (QIIME) and Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt). Our results showed that different relative abundance of certain bacterial taxa between psoriasis patients and healthy individuals, including Faecalibacterium and Megamonas, were increased in patients with psoriasis. It’s also implicated that many cytokines act as main effect molecules in the pathology of psoriasis. We selected the inflammation-related indicators that were abnormal in psoriasis patients and found the microbiome variations were associated with the level of them, especially interleukin-2 receptor showed a positive relationship with Phascolarctobacterium and a negative relationship with the Dialister. The relative abundance of Phascolarctobacterium and Dialister can be regard as predictors of psoriasis activity. The correlation analysis based on microbiota and Inflammation-related indicators showed that microbiota dysbiosis might induce an abnormal immune response in psoriasis. CONCLUSIONS: We concluded that the gut microbiome composition in psoriasis patients has been altered markedly and provides evidence to understand the relationship between gut microbiota and psoriasis. More mechanistic experiments are needed to determine whether the differences observed in gut microbiota are the cause or consequences of psoriasis and whether the relationship between gut microbiota and cytokines was involved. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-021-02125-1. |
format | Online Article Text |
id | pubmed-7941898 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-79418982021-03-09 Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients Zhang, Xinyue Shi, Linjing Sun, Ting Guo, Kun Geng, Songmei BMC Microbiol Research Article BACKGROUND: Psoriasis is an inflammatory skin disease associated with multiple comorbidities and substantially diminishes patients’ quality of life. The gut microbiome has become a hot topic in psoriasis as it has been shown to affect both allergy and autoimmunity diseases in recent studies. Our objective was to identify differences in the fecal microbial composition of patients with psoriasis compared with healthy individuals to unravel the microbiota profiling in this autoimmune disease. RESULTS: We collected fecal samples from 30 psoriasis patients and 30 healthy controls, sequenced them by 16S rRNA high-throughput sequencing, and identified the gut microbial composition using bioinformatic analyses including Quantitative Insights into Microbial Ecology (QIIME) and Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt). Our results showed that different relative abundance of certain bacterial taxa between psoriasis patients and healthy individuals, including Faecalibacterium and Megamonas, were increased in patients with psoriasis. It’s also implicated that many cytokines act as main effect molecules in the pathology of psoriasis. We selected the inflammation-related indicators that were abnormal in psoriasis patients and found the microbiome variations were associated with the level of them, especially interleukin-2 receptor showed a positive relationship with Phascolarctobacterium and a negative relationship with the Dialister. The relative abundance of Phascolarctobacterium and Dialister can be regard as predictors of psoriasis activity. The correlation analysis based on microbiota and Inflammation-related indicators showed that microbiota dysbiosis might induce an abnormal immune response in psoriasis. CONCLUSIONS: We concluded that the gut microbiome composition in psoriasis patients has been altered markedly and provides evidence to understand the relationship between gut microbiota and psoriasis. More mechanistic experiments are needed to determine whether the differences observed in gut microbiota are the cause or consequences of psoriasis and whether the relationship between gut microbiota and cytokines was involved. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-021-02125-1. BioMed Central 2021-03-08 /pmc/articles/PMC7941898/ /pubmed/33685393 http://dx.doi.org/10.1186/s12866-021-02125-1 Text en © The Author(s) 2021 Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Article Zhang, Xinyue Shi, Linjing Sun, Ting Guo, Kun Geng, Songmei Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients |
title | Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients |
title_full | Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients |
title_fullStr | Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients |
title_full_unstemmed | Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients |
title_short | Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients |
title_sort | dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7941898/ https://www.ncbi.nlm.nih.gov/pubmed/33685393 http://dx.doi.org/10.1186/s12866-021-02125-1 |
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