Journal: Arthritis & rheumatology (Hoboken, N.J.)

Article Title: Pathogenesis of diffuse alveolar hemorrhage in murine lupus

doi: 10.1002/art.40077

Figure Lengend Snippet: A, Wild type (WT) and B6 μMT mice were treated with pristane and lungs were examined 14-d later. Some μMT mice received human IgM (50 or 200 μg i.v.) or murine IgG (200 μg i.v.) before pristane treatment (n = 4–6 per group). Left, gross lung pathology; right, prevalence of DAH. B, WT (n = 7), B6 C3−/− (n = 12), and B6 CD18−/− (n = 4) mice were treated with pristane and lungs were examined for DAH 14-d later. Some WT mice were treated with cobra venom factor (CVF) to deplete complement 1-d before (X1, n = 6) or 1-d before and 7-d after (X2, n = 10) pristane. Left, gross lung pathology; right, prevalence of DAH. C, H&E staining of lung tissue from an SLE patient with DAH (upper left) and a WT mouse with pristane-induced DAH (upper right and lower left). Lungs show bland hemorrhage (H), neutrophil-predominant small vessel vasculitis (V), and hemosiderin-laden macrophages (MΦ, arrows). These pathological changes were absent in lungs from pristane-treated C3−/− mice (lower right). Murine lung was examined 14-d after pristane treatment. ***, p < 0.001 vs. WT, Fisher exact test; **** p < 0.001 vs. μMT, Fisher exact test

Article Snippet: Mice were treated with CVF (CompTech, Tyler, Texas) 10 μg i.p. 1-d before and 7-d after pristane treatment.

Techniques: Combined Bisulfite Restriction Analysis Assay, Staining