ABSTRACT
Particulate glucan, a beta-1,3-linked polyglucose derived from Saccharomyces cerevisiae, has been demonstrated to have a wide range of immunopotentiating effects. Glucan administration is associated with the modification of a variety of experimentally induced infectious disease states as well as the inhibition of growth of implantable and spontaneous tumors. The present study was designed to evaluate the effect of glucan upon activation of the complement system in rats and guinea pigs. Additional studies were performed to determine the in vitro activating effect of glucan and zymosan on complement activity of human serum. Glucan activated both the classical pathway of normal human sera and the alternate pathways in C2hu-deficient sera in vitro releasing anaphylatoxins such as C3a. The intravenous injection of glucan activated the alternate pathway of guinea pig plasma. The influence of glucan on complement depletion induced by cobra venom factor (CVF) was also ascertained. Complement activation by glucan may contribute, in part, to the enhanced resistance of the host against tumor growth as well as infectious episodes.
Subject(s)
Complement Activation/drug effects , Glucans/pharmacology , beta-Glucans , Animals , Complement C2/biosynthesis , Complement C3/biosynthesis , Complement C3a , Guinea Pigs , Humans , Rats , Rats, Inbred Strains , Zymosan/pharmacologyABSTRACT
The requirements of complement (C) to induce systemic and cutaneous Forssman reactions were studied in inbred DHC-BA and Hartley strain guinea pigs. After intravenous injection of Forssman antibody, fatal systemic shock was associated with a marked drop in CH50, C4, and C3 and a lesser decrease in C5 hemolytic activity. Platelet counts and leukocyte counts dropped as well. With the use of the purified low molecular weight factor from cobra venom (CVF) to deplete C3, guinea pigs with less than 1% intravascular C3 were protected from lethal shock. Approximately 1% to 3% C3 activity is required for Forssman cutaneous vasculitis. These results confirm earlier studies that classical complement pathway activation occurs in Forssman shock and demonstrate the exquisite biologic efficiency of C3 in provoking the shock syndrome.
Subject(s)
Anaphylaxis/immunology , Complement C3 , Complement System Proteins , Forssman Antigen , Hemorrhage/immunology , Skin Diseases/immunology , Vascular Diseases/immunology , Anaphylatoxins/immunology , Animals , Antibodies , Antigen-Antibody Reactions , Blood Platelets/immunology , Complement C3/analysis , Complement C4/analysis , Complement C5/analysis , Complement System Proteins/analysis , Guinea Pigs , Leukocytes/immunology , Lung Diseases/immunology , Snake Venoms/pharmacology , Time FactorsSubject(s)
Arthritis, Rheumatoid/immunology , Complement System Proteins/metabolism , Lupus Erythematosus, Systemic/immunology , Pleural Effusion/immunology , Centrifugation, Density Gradient , Complement C1/metabolism , Complement C1 Inactivator Proteins , Complement C2/metabolism , Complement Fixation Tests , HumansABSTRACT
Hypersensitivity to procarbazine associated with urticaria, angioedema, and painful joint swelling was found in a 20-year-old student being treated for Hodgkin's disease. A marked fall in complement component activity occurred simultaneously with the development of symtoms. It is suggested that generation of products of complement component activation could be important in the pathogenesis of hypersensitivity to some drugs.
