Complement ratios C3bc/C3 and sC5b-9/C5 do not increase the sensitivity of detecting acute complement activation systemically.


Journal

Molecular immunology
ISSN: 1872-9142
Titre abrégé: Mol Immunol
Pays: England
ID NLM: 7905289

Informations de publication

Date de publication:
01 2022
Historique:
received: 30 08 2021
revised: 08 11 2021
accepted: 21 11 2021
pubmed: 16 12 2021
medline: 22 2 2022
entrez: 15 12 2021
Statut: ppublish

Résumé

Complement activation plays an important pathogenic role in numerous diseases. The ratio between an activation product and its parent protein is suggested to be more sensitive to detect complement activation than the activation product itself. In the present study we explored whether the ratio between the activation product and the parent protein for C3 (C3bc/C3) and for C5 (sC5b-9/C5) increased the sensitivity to detect complement activation in acute clinical settings compared to the activation product alone. Samples from patients with acute heart failure following ST-elevated myocardial infarction (STEMI) and from patients with out-of-hospital cardiac arrest (OHCA) were used. C3, C3bc and C5, sC5b-9 were analysed in 629 and 672 patient samples, respectively. Healthy controls (n = 20) served to determine reference cut-off values for activation products and ratios, defined as two SD above the mean. Increased C3bc/C3- and sC5b-9/C5 ratios were vastly dependent on C3bc and sC5b-9. Thus, 99.5 % and 98.1 % of the increased C3bc/C3- and sC5b-9/C5 ratios were solely dependent on increased C3bc and sC5b-9, respectively. Significantly decreased C3 and C5 caused increased ratios in only 3/600 (0.5 %) and 4/319 (1.3 %) samples, respectively. Strong correlations between C3bc and C3bc/C3-ratio and between sC5b-9 and sC5b-9/C5-ratio were found in the STEMI- (r = 0.926 and r = 0.786, respectively) and the OHCA-population (r = 0.908 and r = 0.843, respectively; p < 0.0001 for all). Importantly, sC5b-9 identified worse outcome groups better than sC5b-9/C5-ratio. C3bc and sC5b-9 were sensitive markers of complement activation. The ratios of C3bc/C3 and sC5b-9/C5 did not improve detection of complement activation systemically.

Sections du résumé

BACKGROUND
Complement activation plays an important pathogenic role in numerous diseases. The ratio between an activation product and its parent protein is suggested to be more sensitive to detect complement activation than the activation product itself. In the present study we explored whether the ratio between the activation product and the parent protein for C3 (C3bc/C3) and for C5 (sC5b-9/C5) increased the sensitivity to detect complement activation in acute clinical settings compared to the activation product alone.
MATERIALS AND METHODS
Samples from patients with acute heart failure following ST-elevated myocardial infarction (STEMI) and from patients with out-of-hospital cardiac arrest (OHCA) were used. C3, C3bc and C5, sC5b-9 were analysed in 629 and 672 patient samples, respectively. Healthy controls (n = 20) served to determine reference cut-off values for activation products and ratios, defined as two SD above the mean.
RESULTS
Increased C3bc/C3- and sC5b-9/C5 ratios were vastly dependent on C3bc and sC5b-9. Thus, 99.5 % and 98.1 % of the increased C3bc/C3- and sC5b-9/C5 ratios were solely dependent on increased C3bc and sC5b-9, respectively. Significantly decreased C3 and C5 caused increased ratios in only 3/600 (0.5 %) and 4/319 (1.3 %) samples, respectively. Strong correlations between C3bc and C3bc/C3-ratio and between sC5b-9 and sC5b-9/C5-ratio were found in the STEMI- (r = 0.926 and r = 0.786, respectively) and the OHCA-population (r = 0.908 and r = 0.843, respectively; p < 0.0001 for all). Importantly, sC5b-9 identified worse outcome groups better than sC5b-9/C5-ratio.
CONCLUSION
C3bc and sC5b-9 were sensitive markers of complement activation. The ratios of C3bc/C3 and sC5b-9/C5 did not improve detection of complement activation systemically.

Identifiants

pubmed: 34906905
pii: S0161-5890(21)00326-6
doi: 10.1016/j.molimm.2021.11.016
pii:
doi:

Substances chimiques

C3 beta c 0
C3 protein, human 0
Complement C3 0
Complement C5 0
Complement Membrane Attack Complex 0
Peptide Fragments 0
SC5b-9 protein complex 0
Complement C3b 80295-43-8

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

273-279

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

Anub Mathew Thomas (AM)

Department of Immunology, Oslo University Hospital and University of Oslo, Norway; Department of Neurology, Drammen Hospital, Vestre Viken Hospital Trust, Norway.

Viktoriia Chaban (V)

Department of Immunology, Oslo University Hospital and University of Oslo, Norway.

Søren E Pischke (SE)

Department of Immunology, Oslo University Hospital and University of Oslo, Norway; Division of Emergencies and Critical Care, Oslo University Hospital, Norway.

Hilde Lang Orrem (HL)

Department of Immunology, Oslo University Hospital and University of Oslo, Norway; Division of Emergencies and Critical Care, Oslo University Hospital, Norway.

Vidar Bosnes (V)

Department of Immunology, Section of Medical Immunology, Oslo University Hospital, Oslo, Norway.

Kjetil Sunde (K)

Division of Emergencies and Critical Care, Oslo University Hospital, Norway; Institute of Clinical Medicine, University of Oslo, Norway.

Ingebjørg Seljeflot (I)

Institute of Clinical Medicine, University of Oslo, Norway; Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Norway; Department of Cardiology, Oslo University Hospital, Norway.

Christofer Lundqvist (C)

Institute of Clinical Medicine, University of Oslo, Norway; Department of Neurology, Akershus University Hospital, Oslo, Norway; Health Services Research Unit, Akershus University Hospital, Oslo, Norway.

Espen Rostrup Nakstad (ER)

Norwegian National Unit for CBRNE Medicine, Division of Medicine, Oslo University Hospital, Norway.

Geir Øystein Andersen (GØ)

Department of Cardiology, Oslo University Hospital, Norway.

Camilla Schjalm (C)

Department of Immunology, Oslo University Hospital and University of Oslo, Norway.

Tom Eirik Mollnes (TE)

Department of Immunology, Oslo University Hospital and University of Oslo, Norway; Research Laboratory, Nordland Hospital, Bodø, Norway; K.G. Jebsen TREC, University of Tromsø, Norway; Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.

Andreas Barratt-Due (A)

Department of Immunology, Oslo University Hospital and University of Oslo, Norway; Division of Emergencies and Critical Care, Oslo University Hospital, Norway. Electronic address: andreas.barrattdue@gmail.com.

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