title: Angiogenesis and lymphangiogenesis in bronchial asthma.
abstract: Neovascularization plays a prominent role in inflammation and tissue remodeling in several chronic inflammatory disorders. Vessel number and size, vascular surface area and vascular leakage are all increased in biopsies from patients with asthma. High levels of VEGF and other angiogenic factors have been detected in tissues and biological samples of patients with asthma and correlate with disease activity and inversely with airway hyper-responsiveness. Inflammation in the lung stimulates the growth of new blood vessels and these contribute to the airway obstruction or airway hyper-responsiveness, or both. Effector cells of inflammation (human lung mast cells, basophils, eosinophils, macrophages, etc.) are major sources of a vast array of angiogenic and lymphangiogenic factors. Inhaled corticosteroids reduce vascularity and growth factor expression and might modulate bronchial vascular remodeling in asthma. Specific antagonists to VEGF and other angiogenic factors and their receptors might help to control chronic airway inflammation and vascular remodeling and offer a novel approach for the treatment of chronic inflammatory lung disorders.
authors.affiliation: Department of Clinical Immunology and Allergy, Center for Basic and Clinical Immunology Research (CISI), University of Naples Federico II, Naples.
authors.forename: A
authors.initials: A
authors.lastname: Detoraki
authors.forename: F
authors.initials: F
authors.lastname: Granata
authors.forename: S
authors.initials: S
authors.lastname: Staibano
authors.forename: F W
authors.initials: FW
authors.lastname: Rossi
authors.forename: G
authors.initials: G
authors.lastname: Marone
authors.forename: A
authors.initials: A
authors.lastname: Genovese
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D001980:Bronchi / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology; D002648:Child; D006801:Humans; D042583:Lymphangiogenesis / Q000502:physiology*; D009389:Neovascularization, Pathologic