INHIBITION OF NEUTROPHIL OXIDATIVE-METABOLISM BY TRICHINOSIS PATIENT SERA - PARASITE ORIGIN OR HOST INDUCTION

The presence of sera factors able to inhibit both neutrophil chemotaxi s 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. spir alis newborn larvae in an ADCC system and their major cytotoxic mechan ism is oxidative metabolism products. We evaluated the effect of trich inellosis sera on neutrophil oxidative burst to determine if neutrophi ls are affected by circulating factors during infection. Cells were in cubated with sera from trichinellosis patients. Basal or stimulated Su peroxide Anion (SA) production and chemiluminescence in response to di fferent stimulation (PMA, f-MLP, opsonized yeasts) of neutrophils incu bated with trichinellosis sera were evaluated and compared with those of cells incubated with control sera. The results show that basal SA p roduction was inhibited by 66% of sera and stimulated by 11%. On the c ontrary f-MLP stimulated production was significantly increased by 22% sera, and inhibited by none. Chemiluminescence in response to f-MLP o r 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 stimulat ing 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.