Serum sFas and sFas-Ligand Levels in Childhood Asthma

Abstract

In recent years, an increasing number of observations has lent support to the concept that dysregulation of apoptosis may play a role in the development of airway inflammation in asthma. In the present study, serum sFas and soluble Fas ligand (sFasL) levels were measured by enzyme-linked immunosorbent assay (ELISA), during and 2 weeks after the treatment of the acute attack in 15 asthmatic children (range, 2–14 years; median, 5 years) to evaluate the possible role of the Fas-FasL system in asthmatic inflammation. Serum sFas levels of stable asthmatic patients were significantly higher than both the ones with acute attack and the controls (p < 0.001, p < 0.01, respectively). sFas levels were higher in nonatopic asthmatics, both in the acute and stable phases, than those of the atopics. sFasL levels during the acute attack were significantly higher than those of the controls (p < 0.05). sFasL levels of patients receiving inhaler corticosteroid (ICS) treatment were significantly higher than those of the patients who did not receive ICS treatment during the acute attack (p < 0.05). The significant increase of sFas levels in asthmatic children during the stable phase of the disease rather than the acute phase made us consider that antiapoptotic mechanisms such as sFas may have a great role in ongoing persistent chronic inflammation. The increased levels of sFasL in patients with acute asthma may be the reflection of the effort of immune system for limitation of inflammation by increasing apoptosis of inflammatory cells.