Fig. 6

Effect of ERK and p38 inhibitors on polyp formation in mice. a Schematic illustration of the murine NP model. BALB/c mice were treated with ovalbumin (OVA), Staphylococcus enterotoxin B (SEB), and a mixture of p38, ERK inhibitors; i.p. intraperitoneal, i.n. intranasal. b Representative photographs of sinonasal spaces and polypoid lesions stained with H&E in the indicated groups. Asterisk denotes the NP lesions in mouse nasal mucosa. Representative photographs were taken at ×40 magnification. Areas indicated with squares are shown as magnified images. c. d Numbers of polypoid lesions and epithelial disruptions were counted and compared. e Relative IFNG mRNA expression in mucosal tissues from each group of mice was compared. f Protein levels of IFN-γ from nasal fluid were measured by ELISA and compared. g Representative images of immunohistochemistry for neutrophil elastase in each group of mice. Scale bars, 50 μm. h The number of neutrophil elastase positive cells were counted and compared. i, j Relative mRNA expression levels of neutrophil-recruiting chemokines (CXCL1 and CXCL2) from each group of mice were compared. k, l qRT-PCR for CDH1 and ACTA2 in each group of mice. n = 3 for control mice, n = 5 for NP mice, n = 5 for NP mice treated with inhibitor mixture, n = 5 for NP mice treated with dexamethasone (c–e and h–l), n = 6 for control mice, n = 10 for NP mice, n = 10 for NP mice treated with inhibitor mixture, n = 10 for NP mice treated with dexamethasone (f). Statistical significance (c–l) was determined by Kruskal–Wallis tests (P < 0.01), followed by Mann–Whitney U-test for pairwise comparisons. *P < 0.05; **P < 0.01. Data are shown as means ± s.e.m