Enhancement of Antigen-Induced Bronchoconstriction in the Guinea Pig after Intravascular Complement Activation with Cobra Venom Factor

1990 ◽  
Vol 91 (1) ◽  
pp. 86-94 ◽  
Author(s):  
Jean F. Regal
Keyword(s):  
Guinea Pig ◽  
Complement Activation ◽  
Cobra Venom ◽  
Cobra Venom Factor

Effect of complement activation with cobra venom factor on pulmonary vascular permeability

1986 ◽  
Vol 61 (6) ◽  
pp. 2202-2209 ◽  
Author(s):  
A. Johnson ◽  
J. A. Cooper ◽  
A. B. Malik
Keyword(s):  
Vascular Permeability ◽  
Plasma Protein ◽  
Complement Activation ◽  
Concentration Ratio ◽  
Protein Concentration ◽  
Cobra Venom ◽  
Plasma Protein Concentration ◽  
Cobra Venom Factor ◽  
Pulmonary Vascular Permeability ◽  
Protein Clearance

We examined the effect of acute complement activation on lung vascular permeability to proteins in awake sheep prepared with lung lymph fistulas. Complement was activated by cobra venom factor (CVF) infusion (400 U/kg for 1 h iv). Studies were made in two groups of sheep: 1) infusion of CVF containing the endogenous phospholipase A2 (PLA2) (n = 6); and 2) infusion of CVF pretreated with bromophenacyl bromide to inhibit PLA2 activity (n = 5). Intravascular complement activation transiently increased mean pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (PVR) in both groups. Pulmonary lymph flow (Qlym) and lymph protein clearance (Qlym X lymph-to-plasma protein concentration ratio) were also transiently increased in both groups. Pulmonary vascular permeability to proteins was assessed by raising left atrial pressure and determining the lymph-to-plasma protein concentration ratio (L/P) at maximal Qlym. In both groups the L/P at maximal Qlym was not different from normal. In a separate group (n = 4), CVF-induced complement activation was associated with 111In-oxine granulocyte sequestration in the lungs. In vitro plasma from CVF-treated animals aggregated neutrophils but did not stimulate neutrophils to produce superoxide anion generation. Therefore, CVF-induced complement activation results in pulmonary neutrophil sequestration and in increases in PVR and lymph protein clearance. The increase in lymph protein clearance is due to increased pulmonary microvascular pressure and not increased vascular permeability to proteins.

scholarly journals C3b-Independent Complement Activation in Ischemia/Reperfusion Mesenteric Tissue Injury in Autoimmune Prone (B6.MRL/lpr) Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-9
Author(s):  
J. Tofferi ◽  
S. Peng ◽  
C. M. Moratz
Keyword(s):  
Lupus Erythematosus ◽  
Complement Activation ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cobra Venom ◽  
Cobra Venom Factor ◽  
Inflammatory Tissue

Complement plays a critical role in the development of tissue injury in systemic lupus erythematosus. The B6.MRL/lpr mouse, an autoimmune prone mouse, exhibits accelerated and intensified tissue injury in the ischemia/reperfusion (IR) model. It has been demonstrated in nonautoimmune mice that inhibition of complement attenuates inflammatory tissue injury in IR models. The role of complement is not as clear in the B6.MRL/lpr strain. B6.MRL/lpr-C3 deficient animals are susceptible to injury, but long-term use of C3 inhibitors in B6.MRL/lpr-C3 competent animals restrained the development of nephritis. To clarify the role of complement in the B6.MRL/lpr strain, initial and midpathway inhibitors were evaluated. C1 inhibition attenuated tissue injury, thrombin deposition, and C5a generation in the B6.MRL/lpr strain. Downstream of C1 inhibition of C3 activation by administration of cobra venom factor suppressed IR injury in immune competent mice, but was not as effective in B6.MRL/lpr mice. C3 levels in both strains were decreased after cobra venom factor treatment; however, C5a generation, thrombin deposition, and tissue injury were observed in the B6.MRL/lpr strain. These studies suggest that in the B6.MRL/lpr autoimmune prone strain C1 activation leads to C3-dependent and C3-independent pathways of complement activation.

Possible role of glucocorticoids in a complement-activated state induced by cobra venom factor in rats

1986 ◽  
Vol 112 (1) ◽  
pp. 122-129 ◽  
Author(s):  
Kiwao Nakano ◽  
Seiji Suzuki ◽  
Oh Chanho ◽  
Kazuo Yamashita
Keyword(s):  
Complement Activation ◽  
Serum Levels ◽  
Iron Chelator ◽  
Cobra Venom ◽  
Cyclooxygenase Inhibitors ◽  
Cobra Venom Factor ◽  
Deferoxamine Mesylate ◽  
Thromboxane Synthetase ◽  
Activated State

Abstract. Activation of the complement system of adrenalectomized rats with an injection of cobra venom factor (CVF) caused death of the rats within 2.5 h. Morphologically, this activation provoked distinct congestion of the gastric glandular mucosa and pulmonary leukostasis. Pretreatment of the animals with dexamethasone abolished the undesirable responses completely. Injection of CVF to intact rats produced only slight responses, but caused a marked increase in the serum levels of corticosterone. Dexamethasone was found to be replaced by promethazine (H1-antihistamine) or dimethylsulphoxide (scavenger of hydroxyl radicals) but not by indomethacine, ibuprofen (cyclooxygenase inhibitors), deferoxamine mesylate (iron chelator) or imidazole (thromboxane synthetase inhibitor). These results suggest that glucocorticoids protect the animals from the adverse effects of excessive complement activation and that they act as an inhibitor of the production or action of histamine and toxic oxygen products induced by complement activation.

Complement Deposition and Cell Death after Myoblast Transplantation

1998 ◽  
Vol 7 (5) ◽  
pp. 427-434 ◽  
Author(s):  
Daniel Skuk ◽  
Jacques P. Tremblay
Keyword(s):  
Cell Death ◽  
Intracellular Calcium ◽  
Complement Activation ◽  
Early Death ◽  
Cobra Venom ◽  
Cobra Venom Factor ◽  
Cd1 Mice ◽  
Myoblast Transplantation ◽  
Complement Deposition

One of the problems limiting myoblast transplantation (MT) is the early death of the transplanted cells. Because complement can be fixed by myoblasts in vitro, and because it has the capacity to induce cell lysis, its possible role in the early death of transplanted myoblasts was investigated. CD1 mice and Macaca mulata monkeys were used as recipients for MT. In some mice, C3 was depleted before MT using Cobra Venom Factor. Mice were sacrificed during the first hour and up to 3 days after MT. Monkeys were biopsied 1 to 4 h after MT. Myoblast necrosis was assessed by the presence of intracellular calcium. Complement deposition was demonstrated by immunohistochemistry with anti-C3 and anti-C5b-9 neoantigen antibodies. In mice, C3 deposition was observed in damaged muscle fibers and in regions containing necrosed myoblasts. Complement depletion did not diminish the proportion of necrosed cells. In monkeys, only a small percentage of transplanted myoblasts showed C3 or C5b-9 deposition, mostly intracellular. Complement activation seems not to be implicated in directly damaging the transplanted cells, but seems secondary to cellular death. Taking into account its chemotactic functions, complement could be implicated in the migration of neutrophils and macrophages into the clusters of transplanted cells. © 1998 Elsevier Science Inc.

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