This study investigated the effects of acute and chronic stress models on the functional capacity of blood neutrophils in beef steers. Steers (n = 32; 209 ± 8 kg) were blocked by BW and assigned to 1 of 3 treatments: (1) Control (CON), no dexamethasone (DEX); (2) Chronic stress (CHR), 0.5 mg/kg BW DEX administered i.v. at 1000 h on d 3 to 6; or (3) Acute stress (ACU), 0.5 mg/kg BW DEX administered i.v. at 1000 h on d 6 only. Multiple blood samples were collected from jugular catheters to profile hematology. A blood sample collected at 2 h after the 4th DEX injection in the CHR treatment and 2 h after the only DEX injection in the ACU treatment was analyzed for functional capacities of neutrophils, which included surface expression of L-selectin (CD62-L) and the phagocytic and oxidative burst capabilities to an environmental Escherichia coli. There was a treatment × time interaction (P ≤ 0.001) for neutrophil concentrations in peripheral circulation. The concentration of neutrophils increased 24 h after the 1st DEX injection among the CHR steers when compared with CON (10.6 vs. 2.8 ± 0.62 × 10⁶/mL; P ≤ 0.001) and remained greater until 72 h after the 4th DEX injection. Neutrophil concentrations also increased rapidly, within 2 h of the DEX, in the ACU steers. Treatment influenced (P ≤ 0.001) the expression of L-selectin on the surface of neutrophils (119^a, 138^b, and 61^c ± 5.2 MFI) for CON, ACU, and CHR steers, respectively. The percentages of neutrophils phagocytizing and producing an oxidative burst were suppressed (P ≤ 0.001) among the CHR steers only (72^a, 71^a, and 55^b ± 4.2%), whereas the intensity of the oxidative burst was suppressed (P ≤ 0.001) for both ACU and CHR steers (170^a, 131^b, 63^c ± 11.7 MFI) for CON, ACU, and CHR steers, respectively. In contrast, the intensity of neutrophil phagocytosis was not influenced by treatment (P = 0.439). These data indicate that chronic DEX suppresses neutrophil L-selectin as well as neutrophil phagocytosis and oxidative burst, whereas the acute DEX may initially prime neutrophil L-selectin expression although the oxidative burst intensity was already partially suppressed.