Inhibitory effect of prostaglandin E₁ on human neutrophil function

Neutrophils accumulated in the lung are thought to play a pivotal role in the pathogenesis of host auto-injury such as adult respiratory distress syndrome (ARDS). We investigated the effect of prostaglandin E₁ (PGE₁) on several aspects of human neutrophil function. PGE₁ significantly decreased reactive oxygen species (ROS), (O_2-, H₂O₂, OH·) generation by neutrophils as well as neutrophil phagocytosis and chemotaxis. In contrast, the drug did not affect the levels of ROS generated by a cell-free ROS generating system. In addition, intracellular calcium concentrations ([Ca²⁺]i) in neutrophils stimulated by f-Met-Leu-Phe were decreased in the presence of PGE₁. These data suggest that the reduction in ROS production and neutrophil phagocytosis and chemotaxis by PGE₁ may contribute to the effectiveness of the drug in host auto-injury including ARDS. The suppression of the increase in [Ca²⁺]i may at least be responsible for inhibition of these neutrophil functions by PGE₁.