Fig 1: Ang-(1–7) treatment suppressed the expression of Beclin-1 protein and secretions of IL-25 and IL-33 in the IL-13-treated BEAS-2B cells. BEAS-2B cells were transfected with control siRNA or ATG5 siRNA, and then treated with IL-13 for 24 h. The IL-13-treated cells were treated with 20 µM Ang-(1–7) for 24 h, and the PBS treatment was as a control treatment. A Cell viability in different groups was measured using a CCK-8 kit. B Expression of Beclin-1 protein was measured using Western blotting. C Secretion of IL-25 and IL-33 was measured using ELISA kits. ns: no significance. *p < 0.05, **p < 0.01
Fig 2: Ang-(1–7) suppressed the results of ATG5 overexpression in IL-13-induced BEAS-2B cells. The BEAS-2B cells were transfected with ATG5 cDNA or vector control, and treated with IL-13 for 24 h. The ATG5 cDNA-transfected or vector control-transfected cells were treated with 20 µM Ang-(1–7) treatment. A Expression of Beclin-1 protein was measured using Western blotting. B Secretion of IL-25 and IL-33 was measured using ELISA kits. **p < 0.01
Fig 3: IgE and inflammatory cytokine levels between HRV-positive and HRV-negative groups in non-AIT AR subjects. (A) Total serum IgE levels in HRV-positive group (n = 54) vs HRV-negative group (n = 49). (B) Total nasal lavage IgE levels in HRV-positive group (n = 54) vs HRV-negative group (n = 49). (C–F) Nasal lavage levels of CXCL13, IL-25, IL-4, and IL-5 cytokines in HRV-positive group (n = 54) vs HRV-negative group (n = 49). Data are presented as the mean ± SD. *P < 0.05 based on two-tailed Mann–Whitney U-tests (A and B) and two-tailed t-test (C–F).
Fig 4: Transcriptional landscape of human tuft cells in vivo. (A) Two-dimensional embedding of single-cell RNA sequencing data from the human small intestine using Uniform Manifold Approximation and Projection (UMAP). Significant epithelial cell populations are annotated, including tuft cells, enterocytes, intestinal stem cells (ISCs) and transient amplifying (TA) cells, goblet cells and enteroendocrine cells (EECs), and BEST4+ cells. (B) Heatmap showing the expression of the top 50 tuft cell signature genes across intestinal epithelial cell populations. (C) Feature plots illustrating the expression patterns of representative tuft cell–associated marker genes, including POU2F3, FYB1, SH2D6, HCK, SUCNR1, IL25, DCLK1, DCLK2, and PTGS1. (D) Dot plot showing the tuft cell marker expression among epithelial clusters. (E) Gene ontology (GO) enrichment analysis of biological processes associated with differentially expressed genes (DEGs) in tuft cells from human small intestine (SI). (F) Reactome pathway enrichment analysis of DEGs in human SI tuft cells, highlighting signaling pathways related to immune regulation, G protein-mediated events, and lipid metabolism. (G-I) Violin plots show the distribution of gene expression levels for genes associated with G protein-coupled receptor (GPCR) signaling (G), PI3K signaling molecules (H), and calcium flux-associated factors (I) across significant intestinal epithelial cell populations. EEC, enteroendocrine cells; ISC, intestinal stem cells.
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