Abstract
PGE2 is a lipid-signaling molecule with complex roles in both homeostasis and inflammation. Depending on the cellular context, PGE2 may also suppress certain immune responses. In this study, we tested whether PGE2 could inhibit bacterial killing by polymorphonuclear neutrophils (PMN) using a mouse model of foodborne listeriosis. We found that PGE2 pretreatment decreased the ability of PMN harvested from the bone marrow of either BALB/cByJ or C57BL/6J mice to kill Listeria monocytogenes in vitro. PGE2 treatment slowed the migration of PMN toward the chemoattractant leukotriene B4, decreased uptake of L. monocytogenes by PMN, and inhibited the respiratory burst of PMN compared with vehicle-treated cells. When immune cells were isolated from the livers of infected mice and tested directly ex vivo for the presence of PGE2, BALB/cByJ cells produced significantly more than C57BL/6J cells. Together, these data suggest that robust PGE2 production can suppress PMN effector functions, leading to decreased bacterial killing, which may contribute to the innate susceptibility of BALB/cByJ mice to infection with the facultative intracellular bacterial pathogen L. monocytogenes.