The objectives of the study were to investigate the effect of Dexamethasone(Dex) treatment on rabbits' polymorphonuclear leucocytes (PMN) L-selectin expression and the possible mechanisms for the observed effect. 6 rabbits in the treatment group were given one dose of Dex (1 mg/kg) and 5 rabbits were given one dose of placebo (normal saline) as control. All rabbits were given one dose of 5 bromo-2-deoxyuridine (Brdu) 100 mg/kg 24 hours prior to treatment in order to label the bone marrow's PMN. Blood was sampled at baseline, 6th, 12th and 24 hours after treatment and PMN count, L-selectin and CD18 expression were determined. Our result showed that Dex treatment caused a significant increase in the PMN count compared to control (9.05 V 3.38 X 109/l, P = 0.02). This was accompanied by a reciprocal decrease in L-selectin expression. The decrease was not related to PMN activation as the CD18 expression was not increased. Analysis of the Brdu labelled PMN at the 6th hour showed that only 30.4% of the circulating PMN was labelled and therefore originated from bone marrow. The rest of the PMN was from either marginating or circulating pool. Therefore, Dex treatment caused a significant neurtophilia in rabbits which was associated with decreased L-selectin expression. Down regulation of L-selectin synthesis in bone marrow PMN is only one of the possible mechanisms.