چکیده (انگلیسی):

Background: Eosinophils play important roles in the development of asthma exacerbation. Viral infection
is a major cause of asthma exacerbation, and the expression of IFN-g-inducible protein of 10 kDa (IP-10)
and cysteinyl leukotrienes (cysLTs) is up-regulated in virus-induced asthma. As b2-adrenergic agonists,
such as formoterol or salbutamol, are used to treat asthma exacerbation, we examined whether formoterol
or salbutamol could modify eosinophil functions such as adhesiveness, particularly those activated
by cysLTs or IP-10.
Methods: Eosinophils were isolated from the blood of healthy subjects and were pre-incubated with
either formoterol or salbutamol, and subsequently stimulated with IL-5, LTD4, or IP-10. Adhesion of
eosinophils to intercellular cell adhesion molecule (ICAM)-1 was measured using eosinophil peroxidase
assays. The generation of eosinophil superoxide anion (O2
) was examined based on the superoxide
dismutase-inhibitable reduction of cytochrome C. Eosinophil-derived neurotoxin (EDN) release was
evaluated by ELISA as a marker of degranulation.
Results: Neither formoterol nor salbutamol suppressed the spontaneous adhesion of eosinophils to
ICAM-1. However, when eosinophils were activated by IL-5, LTD4, or IP-10, formoterol, but not salbutamol,
suppressed the adhesion to ICAM-1. Formoterol also suppressed IL-5, LTD4, or IP-10 induced
eosinophil O2
 generation or EDN release.
Conclusions: These findings suggest that formoterol, but not salbutamol, suppresses eosinophil functions
enhanced by IL-5, LTD4, or IP-10. As these factors are involved in the development of asthma exacerbation,
our results strongly support the hypothesis that administration of formoterol is a novel strategy
for treating asthma exacerbation.