PREDNISONE INHIBITS LEUKOCYTE GRANULE SECRETION INTO THE ASTHMATIC AIRWAY

Asthmatic subjects ingested prednisone (50 mg) or a placebo one week a part at 8 pm followed by bronchoalveolar lavage (BAL) at 4 am on each occasion, For subjects ingesting the prednisone at 8 pm, the total BAL fluid cell counts at 4 am were not significantly different with eithe r the placebo or prednisone. After cellular pellets were removed, assa ys for lactoferrin (neutrophil secondary granule marker), beta-glucuro nidase (present in eosinophils, macrophages, and neutrophil primary gr anules), lysozyme (neutrophil primary and secondary granules), and maj or basic protein (MBP; eosinophil marker) were performed, Lactoferrin concentrations were 82 +/- 9 ng/ml BAL fluid on placebo and 62 +/- 16 ng/ml on prednisone nights (p = N.S.), beta-glucuronidase was 11 +/- 3 mg/ml on placebo and 3 +/- 1 on prednisone nights (p < .05) whereas l ysozyme was 12 +/- 2 and 5 +/- 1 on placebo and prednisone nights, res pectively (p < .02), A semiquantitative ELISA for MBP revealed a mean 51.2 +/- 10.2% suppression of MBP secretion in the subjects who ingest ed prednisone compared to placebo (p = .03), These observations demons trate that pharmacological concentrations of prednisone prevent releas e of neutrophil and eosinophil granule contents in vivo while having n o effect on the neutrophil secondary granule marker lactoferrin, Thus, prednisone suppresses cell function 8 hrs after it is administered wh ile cell counts remained unchanged.