Fig 1: The levels of serum IL-27 in CAP patients with different prognostic outcomes. (A-E) The levels of serum IL-27 on admission were measured in CAP patients with different prognostic outcomes. (A) The levels of serum IL-27 in CAP patients with mechanical ventilation. (B) The levels of serum IL-27 in CAP patients with vasoactive agents. (C) The level of serum IL-27 in CAP patients with ICU admission. (D) The levels of serum IL-27 in CAP patients with different hospital stays. (E) The levels of serum IL-27 in dead cases and survived patients. All data were expressed as mean ± SEM. **P < 0.01.
Fig 2: The levels of serum IL-27 in CAP patients and healthy volunteers. (A-G) Serum IL-27 was determined using ELISA in CAP patients and control subjects. (A) The levels of serum IL-27 in CAP patients and control cases. (B) The levels of serum IL-27 in patients with different CRB-65 scores. (C) The levels of serum IL-27 in patients with different CURB-65 scores. (D) The levels of serum IL-27 in patients with different CURXO scores. (E) The levels of serum IL-27 in patients with different SMART-COP score. (F) The levels of serum IL-27 in patients with different PSI scores. (G) The levels of serum IL-27 in patients with different APACHE Ⅱ scores. All data were expressed as mean ± SEM. *P < 0.05, **P < 0.01.
Fig 3: Integrative transcriptomic analysis of IL-27 in the orbital connective tissues of TAO(A and B) ssGSVA for immune infiltration; correlation between IL-27 and CD56dim natural killer cells.(C) The cluster dendrogram of WGCNA analysis.(D) The soft threshold power (left) and mean connectivity (right) of WGCNA.(E) 7 modules revealed by the WGCNA.(F and G) GO and KEGG analysis based on the blue module of WGCNA.(H) Cistrome DB analysis for transcription factor prediction.
Fig 4: IL-27 inhibited fibrosis progression through the MAPK pathway in TAO(A and B) IHC staining for fibrosis markers (n = 4). Scale bars, 50 μm (40×).(C and D) Immunoblot analysis of the selected proteins under the treatment of IL-27 and IGF-1(n = 3).(E and F) Immunoblot analysis of the selected proteins under the treatment of IL-27 and TGF-β1 (n = 3).(G–I) Immunoblot analysis of the selected pathway proteins under the treatment of IL-27 and TGF-β1 (n = 3).(J and K) Wound-healing assay of TAO-OFs (n = 3). Scale bars, 500 μm.(L and M) Immunoblot analysis of the indicated proteins (n = 3).(N) GESA-GO analysis based on IL-27 expression in orbital connective tissues from GSE58331.(O) GESA-KEGG analysis based on IL-27 expression in orbital connective tissues from GSE58331. Data are presented as means ± SEM; each data point represents an individual experiment; p value by one way ANOVA with Tukey’s test (D, F, H, I, K, M); unpaired two-tailed t test (B).
Fig 5: IL-27 limited adipogenesis induced by multiple pathways in TAO(A and B) Immunoblot analysis of the indicated proteins in TAO-OFs under the treatment of IGF-1 and IL-27 (n = 3).(C and D) Immunoblot analysis of the indicated pathway proteins (n = 3). (E-F) GESA-GO/KEGG analysis based on IL-27 expression in orbital connective tissues from GSE58331.(G) Oil Red O staining for TAO-OFs under adipogenic differentiation. Scale bars, 100 μm.(H and I) Immunoblot analysis of the indicated proteins (n = 3).(J and K) Immunofluorescence of ROS in OFs (n = 3). Scale bars, 50 μm.(L and M) Flow cytometry for ROS in TAO-OFs (n = 3).(N) GSEA-GO analysis based on IL-27 expression in orbital connective tissues from GSE58331.(O) Immunoblot analysis of the indicated pathway proteins (n = 3).(P) Immunoblot analysis of the indicated pathway proteins (n = 3). Data are presented as means ± SEM; each data point represents an individual experiment; p value by one way ANOVA with Tukey’s test (B, D, I, M, O, and P); unpaired two-tailed t test (K).
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