Functional responses of human neutrophils to sodium sulfite (Na2SO3) in vitro

An influx of neutrophils into the airways is a common feature observed duri ng pulmonary inflammation induced by air pollutants, including sulfur dioxi de and sulfates, in the present study focusing on the in vitro interactions of sodium sulfite (Na2SO3) with human neutrophils, we confirm results indi cating that this sulfite induces superoxide production (O-2(-)) by itself. We demonstrated that this response can occur more rapidly than previously r eported (within 5 min), and that Na2SO3 can act as a priming agent, in a co ncentration-dependent fashion, to the bacterial tripeptide N-formyl-methion ine-leucine-phenylalanine (fMLP) by increasing O-2(-) production. In additi on, our results show that Na2SO3 induces gene expression in human neutrophi ls in a concentration-dependent manner as assessed by incorporation of 5-[H -3] uridine into total RNA. However, it does not induce cell shape changes. We also demonstrated that Na2SO3 does not modulate neutrophil apoptosis no r reverse the well-known delaying effect of granulocyte-macrophage colony-s timulating factor (GM-CSF) on apoptosis. We conclude that Na2SO3 acts rapid ly on neutrophil physiology, within a few minutes with respect to superoxid e production, and a few hours (4 h) with respect to gene expression without altering a biological process such as the rate of apoptosis evaluated afte r a long period of incubation (10 h). We further conclude that Na2SO3-induc ed production of O-2(-) does not drive neutrophils to undergo apoptosis, a mechanism known to occur in other conditions. Therefore, the potential toxi city of Na2SO3 during pulmonary inflammation or lung-associated diseases ma y be related to its ability to induce superoxide production without alterin g neutrophil apoptosis rate.