In vitro exposure of normal O,Rh- PMN to plasma obtained from patients with septic shock results in inhibition of formyl-methionyl-leucyl-phenylalanine stimulated superoxide anion (O2.-) production by 40%. Although all reaction velocities and extent of reaction at 5 min were suppressed, neither lag time preceding O2.- production nor duration of initial velocity linearity was affected. No such inhibition was noted when plasma from healthy controls or nonseptic critically ill patients was utilized in the reaction. These results demonstrate that neutrophils are not only a cause, but also a target of the septic shock host inflammatory response.