Extended Data Fig. 4. Changes of ILC3 may contribute to dysbiosis of fecal microflora under pathological conditions.
(a–d) LPLs were isolated from Npm1+/+ and Npm1+/− mice on day 5 after administration of TNBS. (a) Proportion of ILC3s in Lin− cells. (b) Proportion of IL-22+ ILC3s in the total ILC3 population. Number of ILC3s (c) and IL-22+ ILC3s (d) are shown (Npm1+/+: n = 5 individual mice; Npm1+/−: n = 4 individual mice). (e–h) ILC3s in LPLs of Npm1+/+ and Npm1+/− mice under steady-state. (e) Proportion of ILC3s in Lin− cells. (f) Proportion of IL-22+ ILC3s in the total ILC3 population (n = 6 individual mice). Number of ILC3s (g) and IL-22+ ILC3s (h) are depicted (Npm1+/+: n = 6 individual mice; Npm1+/−: n = 5 individual mice). (i,j) Proportion of NCR+ ILC3s and CCR6+ ILC3s in total ILC3s from Npm1+/+ and Npm1+/− mice under steady-state (i) (n = 5 individual mice) and during DSS-induced colitis (j) (n = 6 individual mice). (k–q) Feces from Npm1+/+ mice and Npm1+/− mice under colitis were collected to analyze intestinal microbiota by 16S rRNA sequencing. (k) Observed operational taxonomic unit (OTU), (l) Chao1 index, (m) Shannon–Wiener diversity index (Shannon index) and (n) principal coordinates analysis (PCoA). (o) Venn diagram of two groups of fecal microbiota. (p) The relative abundance of microbiota at phylum level in the fecal samples. (q) Heatmap analysis of the relative abundance of microbiota at family level in the fecal samples. (n = 6 individual mice). (r–u) Co-housed Npm1+/− and control Npm1+/+ mice were administered 2.5% DSS for 7 days, followed by 3 days of recovery (H2O). Body weight (r), DAI (s) and colon length on day 10 (t,u) were analyzed (n = 5 individual mice). Scale bars: 500 μm (left), 100 μm (right). Data are representative of two independent experiments, shown as the means ± s.e.m., and statistical significance was determined by two-tailed unpaired Student’s t-test (a–h,k–m,u) and two-way ANOVA (i,j) (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).