Abstract
The many and varied pathological, immunological and physiological manifestations of infection withNippostrongylus brasiliensis may be unified by considering the role of leukocyte-generated free oxygen radicals in worm expulsion. Aside from directly damaging the adult stage ofN. brasiliensis and possibly leading to its elimination from the small intestine, free radicals may also damage intestinal cells, thereby contributing to the gut pathology characteristic of infection. γ-Interferon (and possibly tumour necrosis factor) may be involved in the initiation of free radical generation in response toN. brasiliensis and may also contribute to various side effects of infection such as hypertriglyceridaemia and cachexia. γ-Interferon may initiate free radical generation via the agency of protein kinase C, an enzyme that can induce various additional responses including lysosomal enzyme and amine secretion and arachidonic acid metabolism. The possible interactions between these mediators and free radicals are subtle and diverse and may profoundly affect the course of infection.

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