Table 1.
Microbes and inflammatory factors in EAE.
| 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 |
IF: inflammatory factor; GF: germ-free; CC: conventionally colonized; EAE: experimental autoimmune encephalomyelitis; CD: cluster of differentiation; Foxp3: Forkhead box P3; Tregs: regulatory T cells; IFN-γ: interferon-γ; IL: interleukin; RR: relapsing–remitting; MIP: macrophage inflammatory protein; MCP: monocyte chemoattractant protein; KCV: kanamycin, colistin, and vancomycin; TNF-α: tumor necrosis factor-α; PBS: phosphate buffer solution; iNKT cell: invariant natural killer T cell; WT B. fragilis: wild type B. fragilis; △PSA B. fragilis: PSA-deficient B. fragilis; RORγ: RAR-related orphan receptor gamma; T-bet: T-box transcription factor TBX21; DCs: dendritic cell; TGF-β: transform growth factor-β; PSA: polysaccharide A; IRT5: consisting of Lactobacillus casei, Lactobacillus acidophilus, Lactobacillus reuteni, Bifidobacterium bifidum, and Streptococcus thermophiles; LAP+: latency-associated peptide; Hsp: heat shock proteins.