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Elevated soluble ST2 protein levels in sera of patients with asthma with an acute exacerbation.

Authors: Oshikawa, K  Kuroiwa, K  Tago, K  Iwahana, H  Yanagisawa, K  Ohno, S  Tominaga, SI  Sugiyama, Y 
Citation: Oshikawa K, etal., Am J Respir Crit Care Med. 2001 Jul 15;164(2):277-81.
Pubmed: (View Article at PubMed) PMID:11463601
DOI: Full-text: DOI:10.1164/ajrccm.164.2.2008120

Previous studies have reported that ST2 is preferentially expressed on Th2 cells and plays a critical part in controlling airway inflammation in murine models of asthma. However, the clinical role of ST2 in patients with bronchial asthma remains unclear. In our study, we examined 56 patients with atopic asthma in a nonattack phase and 200 nonatopic normal volunteers for healthy control, and analyzed the relationship of their serum ST2 levels to asthma severity, pulmonary function, and laboratory data. Of the 56 patients with atopic asthma, 30 exhibited asthmatic exacerbation, and their serum ST2 levels were also analyzed. The serum ST2 levels were low, but a statistical difference was found between patients with nonattack asthma and the healthy control group (p < 0.05). We also found a differential rise of serum ST2 level that correlates well with the severity of asthma exacerbation. Furthermore, the serum ST2 levels during asthma exacerbation statistically correlated with the percentage of predicted peak expiratory flow (r = -0.634, p = 0.004) and Pa(CO(2)) (r = 0.516, p = 0.003). These results suggest that soluble human ST2 protein in sera may be related to Th2-mediated allergic inflammation inducing acute exacerbation in patients with atopic asthma.


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CRRD Object Information
CRRD ID: 5144237
Created: 2011-08-02
Species: All species
Last Modified: 2011-08-02
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.