Bone marrow–derived PACs were ex vivo exposed to HDME and intravenously transferred into HDME-sensitized mice. In contrast to the recipients of naive PACs, animals injected with HDME-exposed PACs developed airway inflammation, remodeling, and hyperreactivity. (A) Schematic overview of ex vivo transfer of PACs into mice. (B) Increased angiogenesis but not lymphangiogenesis in mice injected with HDME-exposed PACs. The number of vessels per 2,500 μm² area is shown. Scale bar, 400 μm. (C) Angiogenesis and upregulation of PAR-2 and VEGFR3 on endothelial cells in animals receiving naive or HDME-exposed PACs. Number of endothelial cells in identical lung lobes was quantified by flow cytometry using lung single-cell suspension. Blood vessel endothelial cells were defined as CD45^–C90^–CD31⁺. VEGFR3 expression was analyzed by immunohistochemistry and number of VEGFR3⁺ blood cells/field was quantified. (D) Goblet cell metaplasia (black arrows) and eosinophil infiltration (brown arrows) in animals injected with naive or HDME-exposed PACs. (E) Th2 cytokines and airway hyperreactivity in animals receiving naive or HDME-exposed PACs. Mean ± SE values of 4 mice per group are shown. Scale bar, 100 μm. Two-tailed Student’s t test was used in B, C, D, and E. ANOVA was used in H. A linear regression model was used to compare lung resistance in E. The interaction between group and methacholine dose in the linear mixed effects model for log-transformed values demonstrates that there are differing slopes describing the relationships between methacholine and Rrs for the naive PAC and HDME PAC groups (P = 0.009). The estimated slope was 0.033 (95% CI 0.011–0.055) for naive PACs and 0.054 (95% CI 0.040–0.067) for HDME PACs, indicating a greater change in Rrs in response to methacholine for the HDME PAC group. In all panels, a indicates airway.