Neutrophil-mediated lung localization of bacteria: a mechanism for pulmonary injury

The reticuloendothelial system (RES) is thought to ensure organ integrity following trauma, burn, and sepsis by removing potentially embolic particulate matter and blood-borne bacteria from the circulation. Blockade of the RES with foreign colloids is known to result in a consumptive depletion of opsonic fibronectin, which modulates reticuloendothelial function, and an increase in lung localization of test particles. We investigated the role of neutrophils as a contributing factor in the increased localization of blood-borne bacteria in the lung after blockade. RE blockade induced by gelatin-coated colloid particle injection resulted in an acute (15-minute) increase in the number of 51Cr-labeled neutrophils localized in the lung, with return to control levels at 60 minutes after blockade. Fibronectin administration following blockade resulted in a significant (P less than 0.05) prolonged retention of neutrophils in the lung up to 2 hours after blockade. A parallel increase (P less than 0.05) in lung localization of heat-killed 14C-labeled Pseudomonas aeruginosa following colloid-induced RE blockade was observed, and fibronectin further increased the number of bacteria localized in the lung. Experimentally induced neutropenia abrogated the effect of colloid injection on lung localization of bacteria. It is concluded that a particulate load results in simultaneous RE blockade and neutrophil margination in the lung, both of which contribute to the increase in lung localization of bacteria. A mechanism for neutrophil-mediated pulmonary injury related to RE dysfunction following trauma is proposed.