Human brucellosis is caused by infection with certain species of the genus Brucella and is characterized by bacterial persistence and inflammation of many host tissues. Neutrophils are one of the predominant cell types present in the infiltrate of these inflamed tissues, and due to their potential effect on the inflammatory response and tissue damage, direct activation of neutrophils by Brucella abortus might contribute to the pathology associated with human brucellosis. B. abortus expresses outer membrane lipoproteins (Omp) with inflammatory properties on a variety of cell types. This study examines the effect of B. abortus and its lipoproteins on neutrophil functions. B. abortus induced an increment in CD35 and CD11b expression and a decline in CD62L accompanied by IL-8 secretion, a response compatible with neutrophil activation. B. abortus lipoprotein Omp19 (L-Omp19), but not its unlipidated form, mimicked the changes associated with neutrophil activation induced by B. abortus. L-Omp19 primed neutrophils for oxidative burst as well as promoted neutrophil migration and prolonged neutrophil survival. Thus, Brucella lipoproteins possess pro-inflammatory properties that could contribute to the localize tissue injury and inflammation by direct activation of neutrophils. Data presented here, together with our previous results implicate Brucella lipoproteins in the pathogenesis of human brucellosis.