Complement activation in infective endocarditis: correlation with extracardiac manifestations and prognosis

Messias-Reason, Iara; Hayashi, Shirley Yumi; Nisihara, Renato; Kirschfink, Michael

doi:10.1046/j.1365-2249.2002.01772.x

Cited by 24 publications

(12 citation statements)

References 33 publications

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“…SC5b-9 was as active as iTCC at the same concentrations. The concentration range of the active complex is compatible with the levels of SC5-9 found in many pathological conditions (18,28,29). On the basis of these results and given the fact that SC5b-9 is usually detected in the circulation and in the extravascular fluids, we decided to use only this complex in all the other experiments at the concentration of 5 g/ml.…”

Section: Terminal Complement Complexes Induce Endothelial Permeabilizsupporting

confidence: 55%

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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Section: Terminal Complement Complexes Induce Endothelial Permeabilizsupporting

confidence: 55%

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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“…. sC5b‐9 was assessed by ELISA using a monoclonal antibody against a neoepitope , as described previously .…”

Section: Methodsmentioning

confidence: 99%

Monitoring of complement activation biomarkers and eculizumab in complement-mediated renal disorders

Wehling

Amon

Bommer

et al. 2016

Clinical and Experimental Immunology

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SummaryVarious complement-mediated renal disorders are treated currently with the complement inhibitor eculizumab. By blocking the cleavage of C5, this monoclonal antibody prevents cell damage caused by complement-mediated inflammation. We included 23 patients with atypical haemolytic uraemic syndrome (aHUS, n 5 12), C3 glomerulopathies (C3G, n 5 9) and acute antibody-mediated renal graft rejection (AMR, n 5 2), treated with eculizumab in 12 hospitals in Germany. We explored the course of complement activation biomarkers and the benefit of therapeutic drug monitoring of eculizumab. Complement activation was assessed by analysing the haemolytic complement function of the classical (CH50) and the alternative pathway (APH50), C3 and the activation products C3d, C5a and sC5b-9 prior to, 3 and 6 months after eculizumab treatment. Eculizumab concentrations were determined by a newly established specific enzyme-linked immunosorbent assay (ELISA). Serum eculizumab concentrations up to 1082 lg/ml point to drug accumulation, especially in paediatric patients. Loss of the therapeutic antibody via urine with concentrations up to 56 lg/ml correlated with proteinuria. In aHUS patients, effective complement inhibition was demonstrated by significant reductions of CH50, APH50, C3d and sC5b-9 levels, whereas C5a levels were only reduced significantly after 6 months' treatment. C3G patients presented increased C3d and consistently low C3 levels, reflecting ongoing complement activation and consumption at the C3 level, despite eculizumab treatment. A comprehensive complement analysis together with drug monitoring is required to distinguish mode of complement activation and efficacy of eculizumab treatment in distinct renal disorders. Accumulation of the anti-C5 antibody points to the need for a patient-orientated tailored therapy.

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“…However, there are situations that make a firm diagnosis difficult. A prominent example is bacterial endocarditis, which often leads to immune complex disease, 24 and may be accompanied by various immune phenomena.…”

Section: Sle Diagnosismentioning

confidence: 99%

Toward new criteria for systemic lupus erythematosus—a standpoint

Aringer

Dörner

Leuchten

et al. 2016

Lupus

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While clearly different in their aims and means, classification and diagnosis both try to accurately label the disease patients are suffering from. For systemic lupus erythematosus (SLE), this is complicated by the multi-organ nature of the disease and by our incomplete understanding of its pathophysiology. Hallmarks of SLE are the presence of antinuclear antibodies (ANA), and multiple immune-mediated organ symptoms that are largely independent. In an attempt to overcome limitations of the current sets of SLE classification criteria, a new fourphase approach is being developed, which is jointly supported by the European League Against Rheumatism (EULAR) and the American College of Rheumatology (ACR). This review attempts to delineate the performance of the current sets of criteria, the reasons for the decision for classification, and not diagnostic, criteria, and to provide a background of the current approach taken. Lupus (2016) 25, 805-811.

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Complement activation in infective endocarditis: correlation with extracardiac manifestations and prognosis

Cited by 24 publications

References 33 publications

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

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

Monitoring of complement activation biomarkers and eculizumab in complement-mediated renal disorders

Toward new criteria for systemic lupus erythematosus—a standpoint

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