The importance of the airway microvasculature in asthma.
OBJECTIVE
The microvasculature in asthma has been known to contribute to airway-wall thickening and oedema from early post-mortem series. Current concepts of airway inflammation in asthma highlight the importance of the role of the Th2 lymphocyte in the atopic response to aeroallergens, the importance of mast-cell mediators in airway remodelling, potential actions of the vascular response in determining airway thickness and mechanisms of angiogenesis involving endogenous as well as homing progenitor cells with angioblastic potential.


RESULTS
The development of animal models of asthmatic airway inflammation and remodelling have given new insight into mechanisms of angiogenesis in asthma. The central role of vascular endothelial growth factor in angiogenesis, vessel leakage and vascular homeostasis is now recognized. A more recent finding is the influence of this factor in enhancing the Th2 response in airway inflammation. The ability of bone marrow-derived angioblasts to migrate to sites of inflammation and contribute to angiogenesis indicates a pivotal role of stem cells in this process.


CONCLUSIONS
These findings now provide logical links between the inflammatory response, stem-cell mobilization, angiogenesis and airflow obstruction in the remodelled airway of asthma. Future studies examining airway-wall thickness will be able to account for the contribution of the vasculature and airway-wall oedema. Therapies aimed at vascular mechanisms may be useful adjuncts to current treatments and the recognition of stem cells as key players in airway remodelling may provide strategies to reduce fixed airflow obstruction in severe disease.
Wilson
John W
JW
Department of Allergy, Immunology and Respiratory Medicine, Alfred Hospital and Monash Medical School, Prahran, Australia. john.wilson@med.monash.edu.au
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D000818:Animals; D001249:Asthma / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D009389:Neovascularization, Pathologic; D012137:Respiratory System / Q000098:blood supply* / Q000473:pathology; D013234:Stem Cells