Biochemistry of Respiratory Disease, Astra Zeneca, Loughborough, UK 2009: Asthmatic airway remodelling is characterized by an increase number and size of submucosal vessels. Although a consistent and long recognized pathologic finding, the mechanisms of new vessel formation and relation to pathophysiology of asthmatic inflammation has only recently been studied. Angiogenesis is a primary event during the initiation of airway inflammation in asthma, and is linked to mobilization and recruitment of bone-marrow derived endothelial progenitor cells (EPC). Asthmatics have higher numbers of circulating EPC than healthy or atopic individuals. EPC from asthmatics are more proliferative, and have a greater angiogenic potential in endothelial cell tube formation assays as compared to control cells. In an allergen-challenge murine model of asthma, EPC are mobilized from the bone marrow within hours of the 1st challenge, and selectively recruited into the lungs. EPC recruitment is both Th1 ánd Th2 dependent and temporally related to microvessel density, which increases 48 hours after initial allergen challenge. The switch to an angiogenic lung environment occurs days in advance of the influx of inflammatory cells, such as eosinophils. Over weeks of chronic allergen-challenge, EPC mobilization and recruitment continue, and the angiogenic milieu is sustained, long after resolution of the acute inflammatory cell influx. Thus, angiogenic response to allergen is a very early pathologic event and independent of inflammation in asthma.