Abstract
The evidence has been provided that in vitro schistosomula of Schistosoma mansoni activate alternative pathway of complement directly and classical pathway of complement indirectly by binding of IgG antibodies to antigens presented on the schistosomula surfaces.
We had the opportunity to study a patient with left-sided pleural effusion caused by paragonimus. Paragonimus has been said to be present in the pleural space and to have no cyst around its body. We analysed total hemolytic complement titers, levels of complement components, anti-complementary activities and immune complexes in pleural fluids from the patient with paragonimiasis to determine whether paragonimus activates complement system. Total hemolytic complement titers and levels of complement components ware corrected by each corresponding serum titer and each corresponding pleural fluid albumin concentration/serum albumin concentration ratio. Total hemolytic complement titers and levels of three complement components (C1q, C4 and C3) in pleural fluids from the patient with paragonimiasis were lower than each mean value for those in pleural fluids from a group of patients with infectious pleurisy. These were within each mean value for those in pleural fluids from a group of patients with malignant pleurisy, in which complement system, especially classical pathway of complement has been suggested to be activated by malignant tumor cells.
These findings suggested that classical pathway of complement was mainly activated in the pleural space of the patient with paragonimiasis as well as in those of patients with malignant pleurisy. Since immune complexes or anti-complementary activities were not detected in pleural fluids from the patient with paragonimiasis, the complement depletion might be related to the activation of classical pathway of complement by binding of IgG antibodies to antigens presented on the paragonimus surfaces. The possibility was raised that the activation of complement around paragonimus could contribute to killing of paragonimus by eosinophils in the immune host.
