Systemic Sclerosis(SSc)

Panel A Study design. BLM was subcutaneously administered to B6 mice daily to construct an SSc mouse model.

Panel B Skin samples were harvested at the experimental endpoint to evaluate cytokine levels. The SSc model group exhibited elevated levels of Th1 cytokines (TNFα and IFNγ), Th2 cytokine (IL-4), Th17 cytokine (IL-17), profibrotic cytokine (TGF-β1), and proinflammatory cytokine (IL-6).

Panel C Representative images of skin histological staining. Dermal thickness was quantified, and significantly increased dermal thickness was detected in the BLM-induced SSc group.

Panel D Representative images of lung histological staining. Histopathological H&E staining revealed alveolar collapse (red arrow), alveolar epithelial necrosis (black arrow), infiltrated neutrophils (yellow arrow), lymphocytes (blue arrow), foam cells (green arrow), as well as hemorrhage and fibrinous exudation (purple arrow). Statistical analysis demonstrated a significantly higher H&E pathological score in the BLM-induced SSc group.

Data are presented as mean ± SEM; n = 3 mice per group. *P < 0.05, **P < 0.01, unpaired two-tailed t-test.

Panel A HSC-NCG-M mice were administered bleomycin (BLM) to establish the SSc model. Lungs were harvested at the experimental endpoint for immune cell profiling. The BLM-induced group exhibited elevated proportions of monocytes, neutrophils and M2 macrophages.

Panel B The mRNA levels of CCL2, CCL3 and CXCL9 were markedly upregulated in lung tissues from model mice.

Panel C Skin tissues were collected at the endpoint for pathological detection. Representative images of Masson’s trichrome staining are shown.

Panel D Quantitative analysis revealed significantly increased Masson-positive collagen deposition in BLM-challenged mice.

Panel E The mRNA levels of the profibrotic markers CCL2 and TGF-β were elevated in skin tissues isolated from BLM-induced mice.

Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P<0.001, unpaired two-tailed t-test.

Panel A Study Design. HOCl was topically applied to the dorsal skin of BALB/c mice to establish the SSc mouse model.

Panel B No significant changes in body weight were observed throughout the experimental period. Skin thickness rose markedly over time following HOCl administration.

Panel C Skin tissues were harvested at the experimental endpoint for molecular detection. Th1 cytokines (TNFα and IFNγ) and the Th2 cytokine, IL-4, exhibited upward trends in the model group. The pro-inflammatory cytokine, IL-6, and profibrotic factor, TGF-β, were significantly upregulated in model mice. Meanwhile, CCL5, CXCL10, CCL2 and STING were substantially elevated, while OSM, PD1 and TREM1 displayed increasing trends in the HOCl-induced group.

Panel D Serum galectin-3 concentrations were significantly elevated in mice subjected to HOCl treatment.

Panel E Masson’s trichrome staining demonstrated prominent dermal thickening in the HOCl-induced SSc group.

Panel F Representative histopathological images. Labels: epidermal thickening (blue arrow); hyperkeratosis (orange arrow); dermal degeneration and necrosis (yellow arrow); degeneration and necrosis of the subcutaneous adipose and muscle layers (light green arrow); reduced or absent skin appendages (dark blue arrow); lymphocyte infiltration (dark red arrow); neutrophil infiltration (black arrow); fibrous tissue hyperplasia (red arrow); homogeneous collagen proliferation (purple arrow); neovascularization (light gray arrow). Scale bars: top row = 200 μm; bottom row = 50 μm. Quantitative scoring revealed a markedly higher inflammatory score in the SSc model group.

Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P<0.001, unpaired two-tailed t-test.