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

• Main Authors: Mengchen Guo, Huixia Wang, Sixie Xu, Yaoyao Zhuang, Jingang An, Chuan Su, Yankai Xia, Jingyun Chen, Zhenjiang Zech Xu, Qisha Liu, Jianwei Wang, Zhou Dan, Kun Chen, Xiaoting Luan, Zhi Liu, Kangjian Liu, Faming Zhang, Yumin Xia, Xingyin Liu
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2020-11-01
• Series: Gut Microbes
• Subjects: systemic lupus erythematosus (sle); gut microbiota; cytokines; glucocorticoid; autoimmune disease
• Online Access: http://dx.doi.org/10.1080/19490976.2020.1768644

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.