Alteration in gut microbiota is associated with dysregulation of cytokines and glucocorticoid therapy in systemic lupus erythematosus

被引:88
作者
Guo, Mengchen [1 ,2 ,3 ]
Wang, Huixia [4 ]
Xu, Sixie [1 ]
Zhuang, Yaoyao [1 ]
An, Jingang [4 ]
Su, Chuan [1 ]
Xia, Yankai [5 ]
Chen, Jingyun [4 ]
Xu, Zhenjiang Zech [6 ]
Liu, Qisha [1 ,2 ,3 ]
Wang, Jianwei [1 ,2 ,3 ]
Dan, Zhou [1 ,2 ,3 ]
Chen, Kun [1 ]
Luan, Xiaoting [1 ]
Liu, Zhi [1 ]
Liu, Kangjian [3 ]
Zhang, Faming [3 ]
Xia, Yumin [4 ]
Liu, Xingyin [1 ,2 ,3 ]
机构
[1] Nanjing Med Univ, Ctr Global Hlth, Key Lab Pathogen Biol Jiangsu Prov, State Key Lab Reprod Med,Microbiol Div,Dept Patho, Nanjing 211166, Peoples R China
[2] Nanjing Med Univ, Key Lab Human Funct Genom Jiangsu Prov, Nanjing, Peoples R China
[3] Nanjing Med Univ, Key Lab Holist Integrat Enterol, Affiliated Hosp 2, Med Ctr Digest Dis, Nanjing, Peoples R China
[4] Xi An Jiao Tong Univ, Sch Med, Affiliated Hosp 2, Dept Dermatol, Xian 710004, Peoples R China
[5] Inst Toxicol, State Key Lab Reprod Med, Nanjing, Peoples R China
[6] Nanchang Univ, Key Lab Food Sci & Technol, Sch Food & Technol State, Nanchang, Jiangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Systemic lupus erythematosus (SLE); gut microbiota; cytokines; glucocorticoid; autoimmune disease; EPIDEMIOLOGY;
D O I
10.1080/19490976.2020.1768644
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
A growing corpus of evidence implicates the involvement of the commensal microbiota and immune cytokines in the initiation and progression of systemic lupus erythematosus (SLE). Glucocorticoids have been widely used in the treatment of SLE patients, however, glucocorticoid treatment carries a higher risk of other diseases. Using the 16S rRNA technique, we investigated the differences between the gut microbiota associated with the immune cytokines of SLE and relevant glucocorticoid treatment in a female cohort of 20 healthy control subjects (HC), 17 subjects with SLE (SLE-G), and 20 SLE patients having undergone glucocorticoid treatment (SLE+G). We observed that the diversity and structure of the microbial community in SLE+G patients were significantly changed compared to that of SLE-G patients, whereas the gut microbial community of the SLE+G group showed a similarity with the HC group, which implicate that the shift in the gut microbiome could represent a return to homeostasis. Furthermore, the up-regulations of immune cytokines in SLE-G were identified as closely related to gut dysbiosis, which indicates that the overrepresented genera in SLE patients may play roles in regulating expression level of these immune cytokines. This associated analysis of gut microbiota, glucocorticoid therapy, and immune factors might provide novel and insightful clues revealing the pathogenesis of SLE patients.
引用
收藏
页码:1758 / 1773
页数:16
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