Fig. 4: FPNI induces intestinal mucosal immune integrity.

During the eight times of FP or vehicle administration, the food intake (a Ctrl: n = 42; FP: n = 50 biologically independent animals) and body weight (b, Ctrl: n = 45; FP: n = 54 biologically independent animals) were measured once a week after each administration in aged mice. The intestine was isolated from young mice and vehicle or FP-administrated aged mice after the eight times of administration. Representative hematoxylin and eosin (H&E)-stained ileum (c, n = 3 biologically independent samples per group). Upper scale bar, 100 μm; Lower scale bar, 50 μm. The expression of aging marker proteins was determined in the intestine tissues by Western blotting with anti-p16^INK4a and anti-p53 antibodies, and the data are represented by the quantitative graphs (d, n = 10 biologically independent samples per group). Secretory immunoglobulin A (SIgA) levels in the feces were analyzed (e, n = 5 biologically independent samples per group), rectal prolapse is presented with quantitative bar graphs (f, O-Ctrl: n = 36; O-FP: n = 43 biologically independent animals), TLR5 protein levels in the intestine (g, n = 10 biologically independent samples per group), TLR5 surface expression in CD11c⁺ LPDCs (h, n = 7 biologically independent samples per group), IL-22 cytokine levels in tissue explants were analyzed after 5 h of incubation (i, O-Ctrl: n = 6; O-FP: n = 7 biologically independent samples). Error bars represent mean ± SEM. ^*P < 0.05. ^**P < 0.01^{, ***}P < 0.001 using the two-tailed Student’s t-test (a), the one-way ANOVA (d), and the two-tailed Mann-Whitney U test (e–i). ns, not significant; PspA, surface protein A of Streptococcus pneumonia; LPDC, lamina propria dendritic cells. Source data are provided as a Source Data file.