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. 2019 Jul 2;39(7):BSR20190228.
doi: 10.1042/BSR20190228. Print 2019 Jul 31.

Mechanism of gut microbiota and Axl/SOCS3 in experimental autoimmune encephalomyelitis

Xiao-Ling Li  1 , Bo Zhang  2 , Meng-Jiao Sun  1 , Cai-Cai Bao  1 , Bo-Yao Yuan  1 , Qin-Fang Xie  1 , Li-Juan Wang  1 , Man-Xia Wang  3
Affiliations

Mechanism of gut microbiota and Axl/SOCS3 in experimental autoimmune encephalomyelitis

Xiao-Ling Li et al. Biosci Rep. .

Abstract

Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system (CNS). The present study explored the role of intestinal microbiota in the initiation and propagation of mice induced by experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. 48 C57BL/6 were randomly divided into control group and EAE group. The changes of body weight and the scores of neurological function were recorded. The mRNA expression of the receptor tyrosine kinase subfamily (AXL) was detected by real-time quantitative PCR. The levels of IL-17 and IFN-γ in blood samples were examined by ELISA. The intestinal microbial composition of mice at different time points during the EAE induction was analyzed by 16S rRNA gene-based sequencing. In EAE group, the body weight began to reduce at day 3 and neurological symptoms began to appear at day 7 after EAE induction. The levels of IL-17 and IFN-γ in EAE group reached the peak at day 21 and then decreased gradually. However, the expression of Axl and SOCS3 reached the lowest level at day 21 and then increased gradually. The microbiome analyses revealed that the abundances of Alistipes, Blautia, and Lachnospiraceae_NK4A136_group were significantly changed at day 14, whereas the abundances of Allobaculum, Eubacterium and Helicobacter were significantly changed at day 30 of EAE induction. The prevotellaceae_NK3B31_group may be key bacteria that contribute to the development of MS. Regulation of intestinal microbiota composition can become a new therapeutic target for the treatment of MS.

Keywords: Gut microbiota; Inflammatory inhibitors; Receptor tyrosine kinase subfamily; experimental autoimmune encephalomyelitis.

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Conflict of interest statement

The authors declare that there are no competing interests associated with the manuscript.

Figures

Figure 1
Figure 1. Changes of neurological function scores in control group and experimental autoimmune encephalomyelitis (EAE) group
Figure 2
Figure 2. Serum cytokine analysis
Serum levels of IL-17 (A) and IFN-γ (B) in control group and experimental autoimmune encephalomyelitis (EAE) group. P represents the comparison of day 12 and 30 with day 21 in EAE group.
Figure 3
Figure 3. Axl and SOCS3 expressions in ventricle of the control group and experimental autoimmune encephalomyelitis (EAE) group
(A) The expression of Axl in brain paraventricular tissues on different days of EAE induction. (B) Axl expression in the paraventricular and cerebellum on day 21 of EAE induction. (C) The expression of SOCS3 on different days of EAE induction.
Figure 4
Figure 4. Analysis of principal component and bacterial composition differences
(A) Principal component analysis (PCA) of the bacterial composition between the control group and experimental autoimmune encephalomyelitis (EAE) group. (B) The differences of bacterial composition at genus level. A–D represent day 7, 14, 21 and 30 after EAE induction in EAE group, respectively. E represents the control group.
Figure 5
Figure 5. The relative abundances and LEfSE analysis
(A) The relative abundances of Alistipes, Blauti, Lachnospiraceae_NK4A136_group, prevotellaceae_NK3B31_group, and prevotellaceae_UCG-001 between the control group (blue-E) and the day 14 of EAE group (red-B). (B) The relative abundances of Allobaculum, Eubacterium, Helicobacter, Parasutterella, and Prevotellaceae between the control group (blue-E) and the day 30 of EAE group (red-D). (C) LEfSE analysis of the bacterial composition on day 7, 14, 21 and 30 of the EAE group. A–D represent day 7, 14, 21 and 30 after EAE induction in EAE group, respectively. E represents the control group.
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