0715 Cell death and damage in paediatric lung disease

A previous summary (0515) deals with the subject of controlled (apoptotic) vs uncontrolled cell death and the implications for chronic organ disease. This relationship between apoptosis and chronic disease has recently become the focus of attention in the context of infantile and paediatric lung disease. However, as is frequently the case, the results do not consistently point in one direction. Surgical correction of congenital heart disease is followed by irreversible pulmonary hypertension in some cases but not in others. In this context, researchers have found that there is a “failure” of endothelial cell apoptosis, and this impairment results in intimal proliferation and irreversible change with consequent pulmonary hypertension. Anti-apoptotic markers are highly expressed, and there is also upregulation of vascular endothelial growth factor with consequential new vessel formation. Similarly, in the context of DPB (diffuse panbronchiolitis), markers show that apoptotic markers are reduced, and uncontrolled cell death/damage predominates, with promotion of T-cell survival, hypercellularity, and diffuse panbronchiolar damage. On the other hand, research into the meconium aspiration syndrome indicates that apoptosis is the more active process. In this situation markers for apoptosis are increased, and addition of a caspase inhibitor reduces lung cell damage and death.

Read more:
J Am Coll Cardiol 2007; 49: 803-10
Respir Med 2006; 100: 2029-36
Life Sci 2005; 76: 1849-58