Detection and Quantification of the Terminal C5b‐9 Complex of Human Complement by a Sensitive Enzyme‐Linked Immunosorbent Assay

Mollnes, T. E.; Lea, Tor; Harboe, Morten

doi:10.1111/j.1365-3083.1984.tb00989.x

Cited by 46 publications

(23 citation statements)

References 20 publications

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“…However, whereas demonstration MAC and contains the S-protein [12] in addi tion to the terminal components. Recently, the fluid-phase TCC has been described in normal human plasma [13] and in increased amounts in patients with activation of com plement in vivo [14], We have observed that some patients have increased plasma levels of both C3d,g and TCC, whereas in others only one of these is increased. In addition, it was observed that C3d,g seemed to increase more rapidly than TCC during storage.…”

Section: Introductionmentioning

confidence: 75%

Early- and Late-Phase Activation of Complement Evaluated by Plasma Levels of C3d,g and the Terminal Complement Complex

Mollnes¹

1985

Complement

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Activation of the initial part (early phase) and terminal part (late phase) of the complement cascade was examined. C3d,g and the fluid-phase terminal complement complex were quantified and compared after spontaneous in vitro activation and after acute in vivo activation caused by extracorporeal circulation during coronary artery surgery. The results suggest that there is a close but not complete correlation between early- and late-phase activation of complement, that C3d,g and the terminal complement complex have different elimination rates in vivo, and that these two indicators are valuable for evaluation of early- and late-phase activation, respectively.

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Section: Introductionmentioning

confidence: 75%

Early- and Late-Phase Activation of Complement Evaluated by Plasma Levels of C3d,g and the Terminal Complement Complex

Mollnes¹

1985

Complement

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“…This assay is based on a monoclonal antibody (aE11) highly specific for a neoepitope exposed in C9 when incorporated into TCC [14,15]. Values are given in arbitrary units (AU) according to a serum standard activated with zymosan, defined to contain 1,000 AU/ml.…”

Section: Methodsmentioning

confidence: 99%

Effects of Natural versus Synthetic Surfactant with SP-B and SP-C Analogs in a Porcine Model of Meconium Aspiration Syndrome

Salvesen¹,

Curstedt

Mollnes

et al. 2013

Neonatology

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Background: Meconium displaces surfactant from the alveolar surface and inhibits its function. The development of active synthetic surfactants is complicated, especially to synthesize the hydrophobic surfactant proteins SP-B and SP-C. A synthetic surfactant, CHF5633 containing SP-B and SP-C analogs, has been designed to act similarly to the natural surfactant poractant alfa. Objective: To test the resistance to meconium inactivation of CHF5633 compared to poractant alfa. Secondary outcome measurements were respiratory and inflammatory parameters. Methods: Twenty-six newborn pigs, bodyweight 1.4-2.0 kg were randomized to receive either poractant alfa or CHF5633. After anesthesia, surgery and final stabilization, meconium was instilled endotracheally followed by surfactant. Bronchial lavage fluid was obtained before intervention and every second hour. Respiratory parameters were registered and blood samples drawn before intervention and every hour. Results: Surfactant was inactivated in both groups 6 h after meconium instillation, but CHF5633 was more resistant than poractant alfa in terms of lipid peroxidation. Respiratory parameters were similar in both groups. Inflammatory and hemostatic parameters differed between groups, suggesting that the surfactants may play different roles in the meconium-induced inflammatory process. Due to the differential effects and complex pattern observed, the data do not indicate that one of the surfactants was superior with respect to inflammatory and hemostatic responses. Conclusion: This study indicates that CHF5633 is as efficient as poractant alfa in experimental meconium aspiration syndrome.

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“…This complex known as SC5b-9, where S stands for S protein or vitronectin, is detected in the circulation and in the extravascular fluid and is commonly regarded as an irrelevant byproduct of C activation (12), although a possible effect of SC5b-9 was postulated by Ishikawa et al (13) in pulmonary hydraulic conductivity. We have previously shown that a cytolytically inactive complex (iTCC), prepared by incubating purified late components and differing from SC5b-9 for the lack of vitronectin and clusterin, despite the inability to lyse target cells, was still able to bind to endothelial cells and to stimulate these cells to express adhesion molecules and tissue factor (14).…”

mentioning

confidence: 99%

Platelet-Activating Factor and Kinin-Dependent Vascular Leakage as a Novel Functional Activity of the Soluble Terminal Complement Complex

Bossi¹,

Fischetti

Pellis³

et al. 2004

The Journal of Immunology

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The infrequent occurrence of septic shock in patients with inherited deficiencies of the terminal complement components experiencing meningococcal disease led us to suspect that the terminal complement complex is involved in vascular leakage. To this end, the permeabilizing effect of the cytolytically inactive soluble terminal complement complex (SC5b-9) was tested in a Transwell system measuring the amount of fluorescein-labeled BSA (FITC-BSA) leaked through a monolayer of endothelial cells. The complex caused increased permeability to FITC-BSA after 15 min as opposed to the prompt response to bradykinin (BK). The effect of SC5b-9 was partially reduced by HOE-140 or CV-3988, two selective antagonists of BK B2 and platelet-activating factor receptors, respectively, and was completely neutralized by the mixture of the two antagonists. Also, DX-88, a specific inhibitor of kallikrein, partially inhibited the activity of SC5b-9. The permeabilizing factor(s) released after 30 min of incubation of endothelial cells with SC5b-9 caused a prompt leakage of albumin like BK. Intravital microscopy confirmed both the extravasation of circulating FITC-BSA across mesenteric microvessels 15 min after topical application of SC5b-9 and the complete neutralization by the mixture of HOE-140 and CV-3988. SC5b-9 induced opening of interendothelial junctions in mesenteric endothelium documented by transmission electron microscopy.

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Detection and Quantification of the Terminal C5b‐9 Complex of Human Complement by a Sensitive Enzyme‐Linked Immunosorbent Assay

Cited by 46 publications

References 20 publications

Early- and Late-Phase Activation of Complement Evaluated by Plasma Levels of C3d,g and the Terminal Complement Complex

Early- and Late-Phase Activation of Complement Evaluated by Plasma Levels of C3d,g and the Terminal Complement Complex

Effects of Natural versus Synthetic Surfactant with SP-B and SP-C Analogs in a Porcine Model of Meconium Aspiration Syndrome

Platelet-Activating Factor and Kinin-Dependent Vascular Leakage as a Novel Functional Activity of the Soluble Terminal Complement Complex

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