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 in | Scientific reports Vol. 6; no. 1; p. 30594 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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02.08.2016
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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. |
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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 |
Author_xml | – sequence: 1 givenname: Xiaofei surname: Liu fullname: Liu, Xiaofei organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University – sequence: 2 givenname: Benhua surname: Zeng fullname: Zeng, Benhua organization: Department of Laboratory Animal Science, College of Basic Medical Sciences, Third Military Medical University – sequence: 3 givenname: Juan surname: Zhang fullname: Zhang, Juan organization: Department of Infectious Diseases, Chongqing Key Laboratory of Infectious Diseases, Southwest Hospital, Third Military Medical University – sequence: 4 givenname: Wenxia surname: Li fullname: Li, Wenxia organization: Department of Laboratory Animal Science, College of Basic Medical Sciences, Third Military Medical University – sequence: 5 givenname: Fangxiang surname: Mou fullname: Mou, Fangxiang organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University – sequence: 6 givenname: Heng surname: Wang fullname: Wang, Heng organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University – sequence: 7 givenname: Qinghua surname: Zou fullname: Zou, Qinghua organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University – sequence: 8 givenname: Bing surname: Zhong fullname: Zhong, Bing organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University – sequence: 9 givenname: Like surname: Wu fullname: Wu, Like organization: Department of Infectious Diseases, Chongqing Key Laboratory of Infectious Diseases, Southwest Hospital, Third Military Medical University – sequence: 10 givenname: Hong surname: Wei fullname: Wei, Hong email: weihong63528@163.com organization: Department of Laboratory Animal Science, College of Basic Medical Sciences, Third Military Medical University – sequence: 11 givenname: Yongfei surname: Fang fullname: Fang, Yongfei email: fangyongfei@qq.com organization: Department of Rheumatology, Southwest Hospital, Third Military Medical University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27481047$$D View this record in MEDLINE/PubMed |
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Title | Role of the Gut Microbiome in Modulating Arthritis Progression in Mice |
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