To address the potential role of the chemokine macrophage inflammatory protein-2 (MIP-2) in airway inflammation, we examined whether MIP-2 may play a role in ozone-induced neutrophilic inflammation of airways and its modulation by dexamethasone in rat lung. Following ozone exposure, MIP-2 mRNA expression in the lung peaked at 2 h after exposure and slowly declined thereafter. Dexamethasone suppressed ozone-induced MIP-2 mRNA expression and neutrophil accumulation in the lung. We suggest that the MIP-2 mRNA induction may switch on the neutrophilic influx observed in this model of lung inflammation. Furthermore, the MIP-2 expression is regulated by dexamethasone which may represent one of the mechanisms by which glucocorticoids exert their potent anti-inflammatory properties.