The effect of anion transport inhibitors and extracellular Cl − concentration on eosinophil respiratory burst activity

Abstract

Furosemide has been shown recently to protect asthmatic patients against certain bronchoconstrictor challenges. We investigated the effect of furosemide on eosinophil function. Since furosemide may be exerting its inhibitory effect on the eosinophil by inhibiting anion transport, we also assessed the effects of the anion transport inhibitors 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). Furosemide, NPPB and DIDS inhibited the eosinophil respiratory burst in response to leukotriene B 4 (LTB 4) and, to a smaller extent, inhibited the response to opsonized zymosan (OZ). To assess whether the anion transport inhibitors were achieving their inhibitory effect by inhibiting an influx of Cl − ions into the eosinophil, the effect of removing extracellular Cl − on eosinophil function was determined. OZ-induced H 2O 2 production was inhibited by removing extracellular Cl − whereas the LTB 4 response was not affected by the concentration of extracellular Cl −.