Background: The CC chemokine eotaxin not only attracts eosinophils to infla
med sites but also promotes adhesion, degranulation and reactive oxygen spe
cies production of eosinophils. Reactive oxygen species released from eosin
ophils are believed to injure epithelial cells at inflamed sites, resulting
in airway hyperresponsiveness. Roxithromycin has been reported to have ant
iasthmatic effects, although its mechanism of action is not thoroughly unde
rstood. Therefore, the effect of roxithromycin on eotaxin-primed reactive o
xygen species production from eosinophils was studied. Methods: Reactive ox
ygen species production by eosinophils cultured with or without roxithromyc
in was evaluted using luminol-dependnet chemiluminescence. Results: Roxithr
omycin inhibited the release of reactive oxygen species from eosinophils ev
oked with the calcium ionophore A23187, regardless of pretreatment with or
without eotaxin. Conclusion: Roxithromycin may protect epithelial cells at
inflamed sites, at least partly by inhibiting the release of reactive oxyge
n species from eosinophils. Copyright (C) 2001 S. Karger AG, Basel.