Fig. 5: P. faecium DSM 32890 exerts metabolic benefits through M2-macrophage polarization.
a,b, Analysis of the small intestine: alternative activated (M2) macrophages (percentage of CD206+ Arg1+ cells from F4/80+ cells) (a) and pro-inflammatory (M1) macrophages (percentage of CD80+ iNOS+ cells from F4/80+ cells) (b) in the total lamina propria cells. c,d, ILC1s (percentage of T-bet+ IFN-γ+ cells from LIN− cells) in total intestinal epithelial cells (c) and mRNA relative expression of IL-22 (d). e–i, Body weight gain (e) and weight of eWAT (f), fasting GIP levels in plasma (g), blood glucose levels after an oral load of glucose (2 g kg−1) (h) and AUC (i). j,k, mRNA relative expression of immune makers (j) and lipid metabolic (k) genes in the eWAT. l–o, Analysis of the microbiota in the caecal content: beta-diversity based on weighted UniFrac distances (l), observed ASVs (m), Shannon diversity index (n) and Inverse Simpson index (o). p–r, Normalized abundance of Akkermansia muciniphila (p), Mucispirillum spp. (q) and Ruminococcaceae_UBA1819 spp. (r). Control, HFHSD and HFHSD + P. faecium n = 8 and HFHSD + P. faecium + GW2580 n = 7. Values are presented as mean ± s.e.m. of n biological replicates shown as individual dots. Significant differences were assessed using one- or two-way ANOVA or Kruskal–Wallis test followed by the corresponding post hoc test. Non-parametric methods were applied for statistical analysis of alpha diversity and differential abundance analysis was performed using the DESeq2 v.1.36 R package. The resulting P values were corrected using the Benjamini–Hochberg (BH) FDR procedure; *P < 0.05. In h, ‘*’ is used when compared to the control diet and ‘#’ when compared to HFHSD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 and #P < 0.05.
