Fig. 2: EPS mouse model exhibits fibrosis, inflammation, and increased vascular density in peritoneum, consisting with the pathological characteristics in human.
From: Targeting STING to disrupt macrophage-mediated adhesion in encapsulating peritoneal sclerosis
A Cross-sectional images of the abdominal cavity in EPS mice, showing widespread, diffuse adhesions forming clot-like structures throughout the peritoneal cavity. Hematoxylin and eosin (HE) and Masson’s trichrome staining of the parietal (B) and visceral (C) peritoneum, demonstrating significant peritoneal thickening and fibrotic deposition in EPS mice. D Immunohistochemical analysis of the parietal peritoneum showing increased expression of extracellular matrix (ECM) markers, including COL1A1, fibronectin (FN), and α-smooth muscle actin (α-SMA), indicative of active fibrosis. E Immunohistochemical analysis of inflammatory markers IL-1β, IL-6, and TNF-α in the parietal peritoneum, showing significant upregulation of these cytokines in EPS mice, highlighting the inflammatory component of the disease. F Immunofluorescent staining of CD31 in the visceral peritoneum (omentum) showing denser angiogenesis in EPS mice compared to controls. Quantification of peritoneal thickness in the parietal (G) and visceral (H) peritoneum, revealing significant thickening in EPS mice (n = 6 per group). I ELISA analysis of peritoneal lavage fluid, confirming an increase in IL-6 levels in EPS mice compared to controls (n = 6 per group). Data are presented as mean ± SEM.*** p < 0.001, two-tailed Student’s t-test.
