Über die Wirkung von Heparin, Heparinoiden und Carrageenin auf die Komponenten des Meerschweinchen-Komplements in vitro

1965 ◽  
Vol 20 (6) ◽  
pp. 575-581 ◽  
Author(s):  
K. Lauenstein ◽  
H. G. Siedentopf ◽  
H. Fischer
Keyword(s):  
Guinea Pig ◽  
Complement System ◽  
Mode Of Action ◽  
Preceding Paper ◽  
Inhibitory Effect ◽  
The Complement System ◽  
Pig Serum

The mode of action of six inhibitors of the complement system of guinea pig serum was analysed by use of the method described in the preceding paper.Carrageenin is the most powerful inhibitor followed by polyvinylalcoholsulfate, polyethenesulfate, heparinoid “Bayer”, dextransulfate, and heparin. All six substances are directed against C′ 1 and C′ 2. Heparin and polyethenesulfate also inhibit C′ 3b,β, while an effect of heparinoid “Bayer”, dextransulfate, and polyvinylalcoholsulfate upon C′ 3b,β could not definitely be demonstrated. It is not clear whether these latter substances act upon C′ 3b,β, C′ 3c,d, or upon both components.All substances tested exert the strongest inhibitory effect upon C′ 1 which thus becomes the limiting component in guinea pig complement.

scholarly journals INTERACTIONS OF THE COMPLEMENT SYSTEM WITH THE SURFACE AND ENDOTOXIC LIPOPOLYSACCHARIDE OF VEILLONELLA ALCALESCENS

1967 ◽  
Vol 125 (5) ◽  
pp. 767-786 ◽  
Author(s):  
Howard A. Bladen ◽  
Henry Gewurz ◽  
Stephan E. Mergenhagen
Keyword(s):  
Cell Surface ◽  
Guinea Pig ◽  
Complement System ◽  
Biological Activities ◽  
Lesion Formation ◽  
Electron Microscopic ◽  
Reaction Conditions ◽  
Microscopic Studies ◽  
The Complement System ◽  
Pig Serum

Electron microscopic studies demonstrated that lesions were produced on the endotoxic lipopolysaccharide (LPS) as well as on the cell surface of V. alcalescens after reaction with fresh guinea pig serum. These lesions were approximately 90 A in diameter, and were seen on two characteristic structural entities derived from LPS preparations after incubation with serum. The use of numerous inhibitors, inactivators, and reaction conditions affecting hemolytic C' activity revealed that these lesions were mediated by the C' system. Concomitant with lesion formation, C' was fixed; the effect on classical C'3 activity was pronounced. It is concluded that endotoxic LPS, as contained in the outer three-layered membrane of the bacterial cell, is a substrate for the C' enzymes. It is suggested that certain biological activities of endotoxin may derive from its effects on the C' system.

scholarly journals Effect of thrombosis on complement activation and neutrophil degranulation during in vitro hemodialysis.

1994 ◽  
Vol 5 (1) ◽  
pp. 110-115
Author(s):  
A K Cheung ◽  
B Faezi-Jenkin ◽  
J K Leypoldt
Keyword(s):  
Complement System ◽  
Complement Activation ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Extracellular Release ◽  
Blood Clots ◽  
Coagulation Proteins ◽  
Neutrophil Degranulation ◽  
The Complement System

Coagulation proteins are known to affect the complement system and neutrophils. To assess the influence of thrombosis on complement and neutrophils during hemodialysis, whole human blood obtained from normal donors and anticoagulated with either 0.8 or 2.0 U/mL of heparin was recirculated for 4 h through cellulose acetate hollow fibers in vitro. Plasma fibrinopeptide A (FPA) levels were measured to assess thrombosis, whereas the activation of the complement system was evaluated at various stages by determining plasma C3a(desArg), C5a(desArg), and SC5b-9 concentrations. The activation of circulating neutrophils was assessed by quantitation of the extracellular release of the intragranular proteins elastase and lactoferrin. Thrombosis was observed when 0.8 U/mL of heparin was used, as indicated by a 36-fold increase in (FPA) levels at 240 min of recirculation and occasional grossly visible blood clots. In contrast, no increase in FPA or clot formation was observed with 2.0 U/mL of heparin. The higher dose of heparin was also associated with a lesser increase in plasma C3a(desArg) and C5a(desArg) concentrations, an observation that is compatible with either an inhibitory effect of heparin or a stimulatory effect of coagulation on the complement system. Plasma elastase or lactoferrin concentrations increased during hemodialysis but were not dependent on heparin dosage at any time. It was concluded that anticoagulation with higher heparin concentration inhibits complement activation in the hemodialysis circuit, but it does not affect neutrophil degranulation.

In vitro-Untersudiungen über Angriffspunkt und Wirkungsunterschiede zum Heparin / In Vitro Studies on the Mode of Action and Differences to Heparin

1971 ◽  
Vol 26 (5) ◽  
pp. 403-408 ◽  
Author(s):  
D. Walb ◽  
M. Loos ◽  
U. Hadding
Keyword(s):  
Complement System ◽  
Mode Of Action ◽  
In Vitro Studies ◽  
The Complement System

The effect of a semisynthetic pentosan-polysulfo-ester (SP 54) upon the complement system in vitro has been studied in comparison with the effects of heparin. Both substances inhibit in small concentrations the Cl-esterase. There are differences in the effect of SP 54 and heparin. According to the in vitro results SP 54 seems to have a ten times higher anticomplementary action. At the same time the influence upon coagulation is less. SP 54 appears to be a substance of therapeutic interest.

Inhibition of Human and Animal Platelet Adhesiveness to Glass Bead Columns by Adenosine, Dipyridamole, Chlorpromazine and Acetylsalicylic Acid

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu
Keyword(s):  
Guinea Pig ◽  
Acetylsalicylic Acid ◽  
Guinea Pigs ◽  
Glass Bead ◽  
Animal Species ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adhesiveness

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.

scholarly journals Interactions of C-reactive protein with the complement system. III. Complement-dependent passive hemolysis initiated by CRP.

1975 ◽  
Vol 142 (5) ◽  
pp. 1065-1077 ◽  
Author(s):  
A.P. Osmand ◽  
R.F. Mortensen ◽  
Joan Siegel ◽  
H. Gewurz
Keyword(s):  
Guinea Pig ◽  
Human Serum ◽  
Complete System ◽  
Gel Filtration ◽  
C Reactive Protein ◽  
Inflammatory Reactions ◽  
Reactive Protein ◽  
Rabbit Igg ◽  
The Complement System ◽  
Pig Serum

Interactions of CRP with various substrates in the presence of human serum have been shown to result in efficient activation of C components C1-C5. We now report the ability of CRP to initiate C-dependent hemolysis. For this purpose CRP was isolated by affinity chromatography using pneumococcal CPS and gel filtration; its purity was established by several criteria. Erythrocytes were coated with CPS (E-CPS) and passively sensitized with CRP. C-dependent lysis of these cells was observed upon the addition of suitably absorbed human serum, and the efficiency of hemolysis compared favorably with that initiated by rabbit IgG anti-CPS antibody. CRP also sensitized E-CPS for lysis by guinea pig C; partial lysis was seen when C4-deficient guinea pig serum was used, suggesting that CRP also shares with antibody the ability of CRP to fully activate the C system and provide further evidence for a role for CRP similar to that of antibody in the initiation and modulation of inflammatory reactions via the complete system.

scholarly journals Anti-GD2 IgA kills tumors by neutrophils without antibody-associated pain in the preclinical treatment of high-risk neuroblastoma

2021 ◽  
Vol 9 (10) ◽  
pp. e003163
Author(s):  
Mitchell Evers ◽  
Marjolein Stip ◽  
Kaylee Keller ◽  
Hanneke Willemen ◽  
Maaike Nederend ◽  
...  
Keyword(s):  
High Risk ◽  
Sensory Neurons ◽  
Complement System ◽  
Severe Pain ◽  
Neuroblastoma Cells ◽  
Antibody Therapy ◽  
Preclinical Treatment ◽  
The Complement System

BackgroundThe addition of monoclonal antibody therapy against GD2 to the treatment of high-risk neuroblastoma led to improved responses in patients. Nevertheless, administration of GD2 antibodies against neuroblastoma is associated with therapy-limiting neuropathic pain. This severe pain is evoked at least partially through complement activation on GD2-expressing sensory neurons.MethodsTo reduce pain while maintaining antitumor activity, we have reformatted the approved GD2 antibody ch14.18 into the IgA1 isotype. This novel reformatted IgA is unable to activate the complement system but efficiently activates leukocytes through the FcαRI (CD89).ResultsIgA GD2 did not activate the complement system in vitro nor induced pain in mice. Importantly, neutrophil-mediated killing of neuroblastoma cells is enhanced with IgA in comparison to IgG, resulting in efficient tumoricidal capacity of the antibody in vitro and in vivo.ConclusionsOur results indicate that employing IgA GD2 as a novel isotype has two major benefits: it halts antibody-induced excruciating pain and improves neutrophil-mediated lysis of neuroblastoma. Thus, we postulate that patients with high-risk neuroblastoma would strongly benefit from IgA GD2 therapy.

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