Inhibition of neutrophil oxidative metabolism by trichinellosis patient sera. Parasite origin or host induction?

The presence of sera factors able to inhibit both neutrophil chemotaxis and phagocytosis was observed in all patients studied at two months from infection caused by Trichinella britovi and in most of them after one year. Human neutrophils with eosinophils are able to kill T. spiralis newborn larvae in an ADCC system and their major cytotoxic mechanism is oxidative metabolism products. We evaluated the effect of trichinellosis sera on neutrophil oxidative burst to determine if neutrophils are affected by circulating factors during infection. Cells were incubated with sera from trichinellosis patients. Basal or stimulated Superoxide Anion (SA) production and chemiluminescence in response to different stimulation (PMA, f-MLP, opsonized yeasts) of neutrophils incubated with trichinellosis sera were evaluated and compared with those of cells incubated with control sera. The results show that basal SA production was inhibited by 66% of sera and stimulated by 11%. On the contrary f-MLP stimulated production was significantly increased by 22% sera, and inhibited by none. Chemiluminescence in response to f-MLP or PMA was inhibited by 46 and 80% of sera, respectively. These results show that trichinellosis sera can modulate not only SA production but also other steps of the oxidative burst, irrespective of the stimulating agent, so suggesting that different neutrophil activation pathways are affected. Increased IL-2 levels observed in most of the sera did not correlate with the inhibiting capacity of sera. The hypothesis of a parasite origin of the inhibiting factors is discussed in the light of host-parasite relationship.