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. Author manuscript; available in PMC: 2017 Jan 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Nov 5;36(1):69–77. doi: 10.1161/ATVBAHA.115.305911

Figure 4.

Figure 4

OVA-induced ALI promotes peri-aortic CaCl2-induced AAA in wild-type mice (panels A–G) and anti-IgE antibody mitigates AAA formation in mice with concurrent productions of ALI and Ang-II infusion-induced AAA in Apoe−/− mice (panels H–K). Aortic diameters from baseline and at harvest, and cross-section AAA lesion area (A), AAA lesion Mac-2+ macrophage content (B), mast cell number (C), media SMC loss in grade (D), and CD31+ microvessel number (E), and BALF total inflammatory cells and lung H&E staining from CaCl2-induced AAA mice sensitized and challenged with OVA or saline. Plasma IgE, IL5, and IL13 (G), plasma IgE (H), aortic diameter and cross-section AAA lesion area at harvest (I), AAA lesion Mac-2+ macrophage content (J), and BALF total inflammatory cell number and lung H&E staining (K) from Apoe−/− mice that had Ang-II infusion-induced AAA and sensitized and challenged with OVA or saline. Representative data for panels B, C, E, F, J, and K are shown to the right. Scale bars: B, C-inset, E, and J: 50 µm. C, F, and K: 200 µm.