Extended Data Fig. 9 |. EcN^Lac characterization.

a, L-LA and D-LA concentration in plasma taken from naive and peak EAE WT mice (n = 5 per group). b, Schematic depicting the genome sequencing of EcN^Lac and parental EcN strains. c, Schematic for the plasmid used to induce ldhA expression in the EcN^Lac engineered strain. d, EcN^GFP reporter strain. e, GFP expression in EcN^GFP after activation at 37C. f,g, D-LA concentration in plasma (f) and colon tissue (g) after EcN^Lac or EcN administration (n = 5–9 mice per group). h, D-LA concentration in CSF and CNS lysate from naive (n = 4–5) and EAE (n = 3) WT mice after EcN^Lac administration, shown relative to D-LA concentration levels in EcN-treated mice. i, Percentage of HIF-1α⁺ DCs out of total DCs isolated from small intestine and colon tissue from EcN (n = 3–5) or EcN^Lac (n = 3–4) treated mice. j,k, Heat map ( j) and GSEA (k) analysis of RNA-seq of DCs isolated from the small intestine of EcN (n = 3) or EcN^Lac (n = 4) treated mice. l,m, EcN^Lac CFUs in blood isolated from naive and peak EAE mice treated with EcN^Lac daily for a week (l) and EcN^GFP in blood 1, 4 and 24 h after oral gavage (m). Small intestine CFU levels are shown as positive controls (n = 4–5 per group). n, Experimental design to assess the effect of EcN^Lac daily or weekly administration on EAE disease course. Statistical analysis was performed using two-way ANOVA with Šídák’s post-hoc test for e,f, and one-way ANOVA with Dunnett’s post-hoc test for selected multiple comparisons for i. Data shown as mean ± s.e.m.