Rationale: Asthmatic airways have an increased number and size of vascular structures, which contribute to airflow obstruction and hyperresponsiveness. Objectives: We examined if pro-angiogenic mediators are elevated in bronchoalveolar lavage fluid (BALf)from asthmatics and if this translated to induction of angiogenesis. Methods: Angiogenic activity in BALf from 12 healthy, non-atopic subjects and 10 mild atopic asthmatics was evaluated by examining tubule formation at 11-days in co-cultures of human endothelial cells with dermal fibroblasts. Vascular structures were visualised by anti-CD31 labeling and quantified by image analysis. Angiogenic growth factors in BALf from healthy and asthmatic subjects were identified using RayBio Antibody Angiogenesis Arrays and by ELISA. Results: Angiogenic activity induced by BALf from healthy subjects was not different from basal tubule formation (p>0.05). However, induction of tubular structures by asthmatic BALf was 2.5-fold greater (p<0.001) compared with healthy. Similarly, levels of pro-angiogenic growth factors (angiogenin, VEGF, MCP-1) were increased ~2.5-fold (p<0.05) in BALf from asthmatics, whereas anti-angiogenic factors (endostatin, Ang-2)were unchanged. A blocking anti-VEGF antibody abolished tubule formation induced by BALf from either healthy or asthmatic subjects (p<0.01). Immunodepletion of VEGF had no effect on basal tubule formation induced by healthy BALf but abrogated enhanced tubule formation by asthmatic BALf (p<0.01). Conclusions: BALf collected from asthmatics but not healthy subjects is functionally active in promoting angiogenesis in vitro. The pro-angiogenic capacity of BALf from asthmatics resides in elevated VEGF derived from asthmatic airways. This observation supports VEGF as a key factor in vascular remodeling in asthma.