Fig 1: Transcriptional profiling of IL-13–dependent genes in the lung after Nippostrongylus brasiliensis infection.Whole lung RNA from WT and Il13−/− mice infected with N. brasiliensis (Nb) on D6pi was analysed by Nanostring. (A) Principle components analysis of naïve and infected WT and Il13−/− mice. (B) Unsupervised, hierarchically clustered heat map of genes differentially expressed between mouse groups with fold change expression level indicated by colour. (C) Columns in each set represent different (biological repeat) mice in each group (C) Predicted upstream regulators from Ingenuity Pathway Analysis. (D) Expression of Foxa2-regulated genes Clca1, Muc5ac, Ccl11, Il33, and Foxa3 were measured in lung tissues on day 2 post-infection and D6pi by quantitative real-time PCR (data normalised against housekeeping gene Rpl13a). (E) Immunofluorescence staining of nuclear IL-33 (magenta) in the parenchyma of the lung and quantification of mean integrated density (IntDen) (scale bar = 100 µm). Data in (A, B, C) are from a single Nanostring run with samples from two to four mice per group. Data (mean ± SEM) in (D, E) were pooled from two individual experiments with three to five mice per group (per experiment). NS, not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (one-way ANOVA and Tukey–Kramer post hoc test).
Fig 2: Plasma levels of sST2 increased with the disease severity in ALD patients. (A‐B) Plasma levels of IL‐33 and sST2 in 20 HCs and 46 ALD patients, including 8 MALD and 38 ALC patients (including 15 patients with ALC+SAH). (C) Correlation analysis of plasma sST2 levels and prognosis scores (MDF scores and MELD scores were calculated for all ALD patients, and Child‐Pugh scores were calculated for ALC patients)
Fig 3: (a) Results of immunohistochemical detection of IL-33 positive area and ST2 positive cells (×200). High magnification photo is in the black square frame (×400). Statistical results were expressed as mean ± SEMs, ###P < 0.001 compared with the normal group; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001 compared with the model group. (b) Detection of the expression of IL-33 protein in mouse dorsal skin tissue by immunohistochemistry. (c) Detection of the expression of ST2 protein in mouse dorsal skin tissue by immunohistochemistry. (①): normal control group; (②): model control group; (③): low-dose QRQS group; (④): middle-dose QRQS group; (⑤): high-dose QRQS group; (⑥): cetirizine medicine group.
Fig 4: The effects of different concentrations of QRQS decoction on the expression of IL-33 mRNA (a) and its receptor IL-1RAcP (b), ST2 (c). Statistical results were expressed as mean ± SEMs, ###P < 0.001, compared with the normal group; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001 compared with the model group.
Fig 5: (a) Effect of QRQS on TNF-α– or TNF-α +IFN-γ-induced HaCaT cells to produce IL-33 mRNA and protein. TNF-α (50 ng/mL) or TNF-α (50 ng/mL) + IFN-γ (50 ng/mL) stimulated HaCaT cells were cultured with different concentrations of QRQS solution for 24 h. RT-PCR was used to detect the IL-33 mRNA secretion. (b) The influence of different time points in different concentration decoctions on the expression of the IL-33 protein. The TNF-α (50 ng/mL) + IFN-γ (50 ng/mL) combined with HaCaT cells were treated with different concentrations (0.125 g/mL, 0.5 g/mL, and 2.0 g/mL) of QRQS, and, at different time points (24, 32, 48, and 56 h), supernatants were collected. The IL-33 protein expression was detected by ELISA. The data are shown as mean ± SEMs, ###P < 0.001, compared with the blank group; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001, compared with the model group.
Supplier Page from Abcam for Anti-IL-33 antibody