|
| Author | Intervention | Function | IF increase | IF decrease | Microbial changes |
|
| Lee et al. [108] | GF mice versus CC mice | Resistant to the development of EAE in GF mice | CD4+ CD25+ Foxp3+ Tregs | IFN-γ and IL-17A | |
| Berer et al. [109] | GF mice versus SPF RR mice | Reduce the percentage of EAE in GF mice | CD4+ T cells | TH17 T-cell receptor (TCRablow) | |
| Ochoa-Reparaz et al. [42] | Antibiotic (ampicillin, neomycin sulfate, metronidazole, vancomycin), minocycline | Protects mice against EAE; reduced the severity of EAE | IL-13, IL-10
FoxP3+ Treg cells
CD4+ or CD8+ T cell | IFN-γ, MIP-1α, MIP-1β, MCP-1, IL-17, and IL-6 | |
| Yokote et al. [110] | Antibiotics (KCV) | Suppressed the development of EAE | | IFN-γ, TNF-α, IL-6, and IL-17
Th17
iNKT cells | Reduction of Lactobacillus murinus and Bacteroides fragilis and increase in Bacteroides thetaiotaomicron |
| Ochoa-Reparaz et al. [114] | (1) Antibiotics
(2) Antibiotics + WT B. fragilis
(3) Antibiotics + △PSA B. fragilis
(4) Mice treated with PBS | (1) Antibiotics: reduce EAE severity; delays clinical onset.
(2) Antibiotics + WT B. fragilis: protect against disease; reduced clinical severity | (1) Antibiotics: IL-13, GATA-3
(2) WT B. fragilis: IL-10, IFN-γ, IL-12, GATA-3, SMAD-3
(3) △PSA B. fragilis: RORγt, IL-17, and T-bet | (1) Antibiotics: T-bet, IFN-γ, IL-17 and IL-6
(2) WT B. fragilis: RORgt, IL-17
(3) △PSA B. fragilis: GATA-3, IL-10, and IL-13 | In WT or △PSA B. fragilis group: increase Bacteroides spp. counts |
| Ochoa-Reparaz et al. [157] | (1) Antibiotic (ampicillin, metronidazole, vancomycin, and neomycin sulfate)
(2) Adoptively transferred CD5+ B cells | Both groups can reduce the severity of EAE | Enhances the frequency of IL-10 producing CD1dhigh CD5+ B cells | | |
| Ochoa-Reparaz et al. [165] | Oral administration with purified PSA | Both prevention and therapeutic effect on EAE | CD103 expressing | | |
| Wang et al. [116, 184] | Treatment with PSA versus PBS | Delayed clinical onset and progression of EAE | CD39+ CD4 T cells
CD39+ Foxp3+ CD4 Tregs | | |
| Jun et al. [122, 123] | Treatment with Salmonella typhimurium | Reduced clinical development and protection against EAE | IL-17, IL-4, IL-10, and IL-13
Th1 and Th17 | TGF-β, IFN-γ, Foxp3+ CD4+ T cells | |
| Ochoa-Reparaz et al. [115] | Treatment with Salmonella typhimurium | Reduced clinical scores and reduced disease duration | CNS inflammatory cell infiltration; CD25+ CD4+ T cells
FoxP3+ Treg cells | | |
| Ezendam et al. [113] | Bifidobacterium animalis | Reduced the duration of clinical symptoms of EAE | | | |
| Ezendam and van Loveren [166] | Lactobacillus casei Shirota | Increased the duration of clinical symptoms of EAE | | | |
| Lavasani et al. [111] | Lactobacilli | Prevents and therapy of EAE | IL-4, IL-10 and TGF-β1
IL-27 | TNF-α, IFN-γ | |
| Takata et al. [118] | P. acidilactici | Prevent and therapy of EAE | CD4+ IL-10 producing cells
CD4+ FoxP3+ cells | | |
| Maassen and Claassen [119] | Lactobacilli | Suppress the disease | | | |
| Kwon et al. [149] | Orally IRT5 | Prevent and therapy of EAE | IL-2, IL-4, IL-10 | Th1/Th17; IFNγ, TNFα, and IL17 | |
| Rezende et al. [170] | L. lactis | Prevented the development of EAE | IL-10, CD4+ FoxP3+ Treg cells and CD4+ LAP+ Tregs | IL-17 | |
| Chitrala et al. [121] | CD44 deletion and fecal transfer | Amelioration of EAE | Change in SCFAs: propionic acid and i-butyric acid | | Dominant in Bacteroidetes phylum and low in Firmicutes phylum. |
| Scott et al. [41] | Omeprazole treatment | No difference in clinical scores | | | Increase unidentified bacteria in S24-7 and decrease in Akkermansia muciniphila and Coprococcus sp. |
| Mangalam et al. [120] | Administration of Prevotella histicola | Suppressed EAE induced | CD4+ FoxP3+ Tregs
DCs, IL-10 | IL-17 and IFN-γ | |
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