K. Oshikawa et al., Elevated soluble ST2 protein levels in sera of patients with asthma with an acute exacerbation, AM J R CRIT, 164(2), 2001, pp. 277-281
Previous studies have reported that ST2 is preferentially expressed on Th2
cells and plays a critical part in controlling airway inflammation in murin
e models of asthma. However, the clinical role of ST2 in patients with bron
chial asthma remains unclear. In our study, we examined 56 patients with at
opic asthma in a nonattack phase and 200 nonatopic normal volunteers for he
althy control, and analyzed the relationship of their serum ST2 levels to a
sthma severity, pulmonary function, and laboratory data. Of the 56 patients
with atopic asthma, 30 exhibited asthmatic exacerbation, and their serum S
T2 levels were also analyzed. The serum ST2 levels were low, but a statisti
cal difference was found between patients with nonattack asthma and the hea
lthy control group (p < 0.05). We also found a differential rise of serum S
T2 level that correlates well with the severity of asthma exacerbation. Fur
thermore, the serum ST2 levels during asthma exacerbation statistically cor
related with the percentage of predicted peak expiratory flow (r = -0.634,
p = 0.004) and Pa-CO2 (r = 0.516, p = 0.003). These results suggest that so
luble human ST2 protein in sera may be related to Th2-mediated allergic inf
lammation inducing acute exacerbation in patients with atopic asthma.