Angiogenesis In children with Bronchial asthma

Abstract

Asthma is a chronic inflammatory disease of the airways, with associated repair processes. Both inflammatory and repair processes appear to be strictly related, and can lead to several histopathological alterations of the bronchial mucosa, such as the shedding of epithelium and increased thickness of the basement membrane. The integrity as well as the alterations of the bronchial structure are the consequence of several biological events, such as cell proliferation and death, cell activation and inhibition, and extra cellular matrix (ECM) production and degradation (1/ignofa et a 1997). Angiogenesis and microvascular remodeling are elements of the tissue repair in chronic inflammatory diseases and tumors. Both types of changes in the microvasculature result from endothelial cell proliferation and often occur together, but they represent different phenomena and responses to different stimuli. Angiogenesis is the growth of new blood vessels from existing ones, whereas microvascular remodeling involves structural alterations-usually enlargement of arterioles, capillaries or venules, without the formation of new vessels (tJJunni[£2001). Many factors can induce angiogenesis including a rang of mediators and growth factors, others can cause vasodilatation and microvascular leakage. It is thought that mast cells play a key role in modulating these vascular remodeling changes by releasing cytokines and growth factors (Wifson, 2005} Angiogenesis is regulated by a balance of angiogenic and antiangiogenic factors (X{agsourn ana'1J'J7L11Wr. 2()()()}. Induced sputum from asthmatic subjects revealed imbala.nce between vascular endothelial growth factor (VEGF) (angiogenic) and endostatin (anti­ angiogenic factor) levels (JJLsai et af., 2002).

In the future novel therapies may be directed towards angiogenesis, vasodilatation and microvascular leakage (Wifson,2005).