Fig. 5

Gut bacterial dysbiosis promotes hyperplasia of tuft cells and secretion of IL-25. a-e An orthotopic C57BL/6 mice hepatic tumor model with gut microflora dysbiosis was prepared as described in the methods. a Images of tumors from each group. b Tumor weight at the time of sacrifice. c Serum level of IL-25 was detected by ELISA in each group. d Concentrations of IL-25 in small intestine and colon tissue homogenates were detected by ELISA. e Tuft cell marker DCLK1 representative IHC images. Statistical data were shown at the right. Bar, 20 μm. f-h 16S rRNA sequencing and analysis of feces gut microbiota of mice. N, normal control group. A, combination antibiotics group (ANMV). C, cefoperazone group. V, vancomycin group. f PCoA score based on weighted unifrac metrics was different in each group. g Observed bacterial species’ richness in feces samples from each group. p < 0.05 by Wilcoxon rank-sum test. h Hierarchical clustering of each group using Bray-Curtis dissimilarity indices at the phylum level by the weighted unifrac distances. i and j Feces suspensions with bacteria from the above groups were used to treat colonic epithelial NCM460 cells. i Western blotting was performed to determine DCLK1 and IL-25 levels. j Immunofluorescence staining was used to detect DCLK1 (red) and IL-25 (green) in slides embedded with NCM460 cells. Representative immunofluorescence images. Bar, 50 μm. k Feces suspensions without bacteria from the above groups were used to treat colonic epithelial NCM460 cells. Western blotting was performed to detect DCLK1 and IL-25 levels. *p < 0.05, **p < 0.01, ***p < 0.001, ns, no significance