Role of the Gut Microbiome in Modulating Arthritis Progression in Mice

Genetics alone cannot explain most cases of rheumatoid arthritis (RA). Thus, investigating environmental factors such as the gut microbiota may provide new insights into the initiation and progression of RA. In this study, we performed 16S rRNA sequencing to characterise the gut microbiota of DBA1 m...

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Published inScientific reports Vol. 6; no. 1; p. 30594
Main Authors Liu, Xiaofei, Zeng, Benhua, Zhang, Juan, Li, Wenxia, Mou, Fangxiang, Wang, Heng, Zou, Qinghua, Zhong, Bing, Wu, Like, Wei, Hong, Fang, Yongfei
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 02.08.2016
Nature Publishing Group
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Abstract Genetics alone cannot explain most cases of rheumatoid arthritis (RA). Thus, investigating environmental factors such as the gut microbiota may provide new insights into the initiation and progression of RA. In this study, we performed 16S rRNA sequencing to characterise the gut microbiota of DBA1 mice that did or did not develop arthritis after induction with collagen. We found that divergence in the distribution of microbiota after induction was pronounced and significant. Mice susceptible to collagen-induced arthritis (CIA) showed enriched operational taxonomic units (OTUs) affiliated with the genus Lactobacillus as the dominant genus prior to arthritis onset. With disease development, the abundance of OTUs affiliated with the families Bacteroidaceae, Lachnospiraceae, and S24-7 increased significantly in CIA-susceptible mice. Notably, germ-free mice conventionalized with the microbiota from CIA-susceptible mice showed a higher frequency of arthritis induction than those conventionalized with the microbiota from CIA-resistant mice. Consistently, the concentration of the cytokine interleukin-17 in serum and the proportions of CD8+T cells and Th17 lymphocytes in the spleen were significantly higher in the former group, whereas the abundances of dendritic cells, B cells, and Treg cells in the spleen were significantly lower. Our results suggest that the gut microbiome influences arthritis susceptibility.
AbstractList Genetics alone cannot explain most cases of rheumatoid arthritis (RA). Thus, investigating environmental factors such as the gut microbiota may provide new insights into the initiation and progression of RA. In this study, we performed 16S rRNA sequencing to characterise the gut microbiota of DBA1 mice that did or did not develop arthritis after induction with collagen. We found that divergence in the distribution of microbiota after induction was pronounced and significant. Mice susceptible to collagen-induced arthritis (CIA) showed enriched operational taxonomic units (OTUs) affiliated with the genus Lactobacillus as the dominant genus prior to arthritis onset. With disease development, the abundance of OTUs affiliated with the families Bacteroidaceae, Lachnospiraceae, and S24-7 increased significantly in CIA-susceptible mice. Notably, germ-free mice conventionalized with the microbiota from CIA-susceptible mice showed a higher frequency of arthritis induction than those conventionalized with the microbiota from CIA-resistant mice. Consistently, the concentration of the cytokine interleukin-17 in serum and the proportions of CD8+T cells and Th17 lymphocytes in the spleen were significantly higher in the former group, whereas the abundances of dendritic cells, B cells, and Treg cells in the spleen were significantly lower. Our results suggest that the gut microbiome influences arthritis susceptibility.
Genetics alone cannot explain most cases of rheumatoid arthritis (RA). Thus, investigating environmental factors such as the gut microbiota may provide new insights into the initiation and progression of RA. In this study, we performed 16S rRNA sequencing to characterise the gut microbiota of DBA1 mice that did or did not develop arthritis after induction with collagen. We found that divergence in the distribution of microbiota after induction was pronounced and significant. Mice susceptible to collagen-induced arthritis (CIA) showed enriched operational taxonomic units (OTUs) affiliated with the genus Lactobacillus as the dominant genus prior to arthritis onset. With disease development, the abundance of OTUs affiliated with the families Bacteroidaceae, Lachnospiraceae, and S24-7 increased significantly in CIA-susceptible mice. Notably, germ-free mice conventionalized with the microbiota from CIA-susceptible mice showed a higher frequency of arthritis induction than those conventionalized with the microbiota from CIA-resistant mice. Consistently, the concentration of the cytokine interleukin-17 in serum and the proportions of CD8+T cells and Th17 lymphocytes in the spleen were significantly higher in the former group, whereas the abundances of dendritic cells, B cells, and Treg cells in the spleen were significantly lower. Our results suggest that the gut microbiome influences arthritis susceptibility.Genetics alone cannot explain most cases of rheumatoid arthritis (RA). Thus, investigating environmental factors such as the gut microbiota may provide new insights into the initiation and progression of RA. In this study, we performed 16S rRNA sequencing to characterise the gut microbiota of DBA1 mice that did or did not develop arthritis after induction with collagen. We found that divergence in the distribution of microbiota after induction was pronounced and significant. Mice susceptible to collagen-induced arthritis (CIA) showed enriched operational taxonomic units (OTUs) affiliated with the genus Lactobacillus as the dominant genus prior to arthritis onset. With disease development, the abundance of OTUs affiliated with the families Bacteroidaceae, Lachnospiraceae, and S24-7 increased significantly in CIA-susceptible mice. Notably, germ-free mice conventionalized with the microbiota from CIA-susceptible mice showed a higher frequency of arthritis induction than those conventionalized with the microbiota from CIA-resistant mice. Consistently, the concentration of the cytokine interleukin-17 in serum and the proportions of CD8+T cells and Th17 lymphocytes in the spleen were significantly higher in the former group, whereas the abundances of dendritic cells, B cells, and Treg cells in the spleen were significantly lower. Our results suggest that the gut microbiome influences arthritis susceptibility.
Genetics alone cannot explain most cases of rheumatoid arthritis (RA). Thus, investigating environmental factors such as the gut microbiota may provide new insights into the initiation and progression of RA. In this study, we performed 16S rRNA sequencing to characterise the gut microbiota of DBA1 mice that did or did not develop arthritis after induction with collagen. We found that divergence in the distribution of microbiota after induction was pronounced and significant. Mice susceptible to collagen-induced arthritis (CIA) showed enriched operational taxonomic units (OTUs) affiliated with the genus Lactobacillus as the dominant genus prior to arthritis onset. With disease development, the abundance of OTUs affiliated with the families Bacteroidaceae, Lachnospiraceae, and S24-7 increased significantly in CIA-susceptible mice. Notably, germ-free mice conventionalized with the microbiota from CIA-susceptible mice showed a higher frequency of arthritis induction than those conventionalized with the microbiota from CIA-resistant mice. Consistently, the concentration of the cytokine interleukin-17 in serum and the proportions of CD8+T cells and Th17 lymphocytes in the spleen were significantly higher in the former group, whereas the abundances of dendritic cells, B cells, and Treg cells in the spleen were significantly lower. Our results suggest that the gut microbiome influences arthritis susceptibility.
ArticleNumber 30594
Author Liu, Xiaofei
Zhang, Juan
Zeng, Benhua
Wu, Like
Li, Wenxia
Fang, Yongfei
Zou, Qinghua
Mou, Fangxiang
Wang, Heng
Zhong, Bing
Wei, Hong
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  organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University
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  fullname: Zeng, Benhua
  organization: Department of Laboratory Animal Science, College of Basic Medical Sciences, Third Military Medical University
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  organization: Department of Infectious Diseases, Chongqing Key Laboratory of Infectious Diseases, Southwest Hospital, Third Military Medical University
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  organization: Department of Laboratory Animal Science, College of Basic Medical Sciences, Third Military Medical University
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  surname: Mou
  fullname: Mou, Fangxiang
  organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University
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  organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University
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  email: fangyongfei@qq.com
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/27481047$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright The Author(s) 2016
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Snippet Genetics alone cannot explain most cases of rheumatoid arthritis (RA). Thus, investigating environmental factors such as the gut microbiota may provide new...
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StartPage 30594
SubjectTerms 13/31
45
45/91
631/326/2565/2134
692/4023/1670/498
Animals
Arthritis
Arthritis, Experimental - chemically induced
Arthritis, Experimental - immunology
Arthritis, Experimental - microbiology
Bacteria - classification
Bacteria - genetics
CD8 antigen
Collagen
Dendritic cells
Digestive system
Disease Models, Animal
Disease Progression
DNA, Bacterial - genetics
DNA, Ribosomal - genetics
Environmental factors
Gastrointestinal Microbiome
Genetics
Germ-Free Life
Germfree
Helper cells
Humanities and Social Sciences
Humans
Interleukin 17
Interleukin-17 - blood
Intestinal microflora
Lymphocytes
Lymphocytes B
Lymphocytes T
Mice
Mice, Inbred DBA
Microbiota
multidisciplinary
Phylogeny
Rheumatoid arthritis
RNA, Ribosomal, 16S - genetics
Rodents
rRNA 16S
Science
Science (multidisciplinary)
Sequence Analysis, DNA - methods
Spleen
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Title Role of the Gut Microbiome in Modulating Arthritis Progression in Mice
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