Differential patterns of circulating adhesion molecules in children with bronchial asthma and acute bronchiolitis.

The object of the study was to assess the levels of circulating forms of the cellular adhesion molecules ICAM-1, VCAM-1, E-selectin, L-selectin and P-selectin in young children with asthma and acute bronchiolitis. Thirty-nine children aged 12 to 84 months with mild or moderate asthma were studied at admission for acute asthma (n = 15) or in a stable phase (n = 24). Ten of the children with acute asthma were seen again after one month. Twenty-two children aged 1 to 17 months with acute bronchiolitis and nine non-atopic controls were also included in the study. In children with acute asthma, the mean concentration of circulating soluble ICAM-1 (sICAM-1) was increased compared to children with stable asthma (mean 442 micrograms/l versus 363 micrograms/l; p < 0.001) and to controls (363 micrograms/l; p < 0.05). The levels of sICAM-1 remained high at follow up. In children with stable asthma, the mean serum concentration of soluble L-selectin (sL-selectin) (2080 micrograms) was significantly higher than in the controls (1664 micrograms/l; p < 0.05). The levels of circulating cellular adhesion molecules were similar in atopic and non-atopic asthmatics. Children with acute bronchiolitis had increased serum levels of soluble VCAM-1 (sVCAM-1) (1637 micrograms/l versus 1019 micrograms/l in the controls; p < 0.01) and sL-selectin (2041 micrograms/l versus 1664 micrograms/l in the controls; p < 0.05). There was no difference between the levels of circulating cellular adhesion molecules in children with respiratory syncytial virus (RSV) positive and RSV negative bronchiolitis. Soluble E-selectin (sE-selectin) and soluble P-selectin (sP-selectin) in serum were not significantly increased in any of the groups studied. In conclusion, our data suggest differential patterns of circulating cellular adhesion molecules in young children with acute asthma, stable asthma, and acute bronchiolitis, which may reflect differences in the underlying inflammatory processes in these obstructive pulmonary diseases.