Effect of dapagliflozin on collectins and complement activation in plasma from patients with type 2 diabetes and albuminuria: Data from the DapKid cohort.

Albuminuria Complement system Lectin cascade SGLT-2 inhibitor Type 2 diabetes mellitus

Journal

Immunobiology
ISSN: 1878-3279
Titre abrégé: Immunobiology
Pays: Netherlands
ID NLM: 8002742

Informations de publication

Date de publication:
15 Mar 2024
Historique:
received: 06 12 2023
revised: 13 03 2024
accepted: 15 03 2024
medline: 23 3 2024
pubmed: 23 3 2024
entrez: 22 3 2024
Statut: aheadofprint

Résumé

Sodium-glucose cotransporter 2 (SGLT- 2) inhibitors exert cardiovascular and kidney-protective effects in people with diabetes. Attenuation of inflammation could be important for systemic protection. The lectin pathway of complement system activation is linked to diabetic nephropathy. We hypothesized that SGLT-2 inhibitors lower the circulating level of pattern-recognition molecules of the lectin cascade and attenuate systemic complement activation. Analysis of paired plasma samples from the DapKid crossover intervention study where patients with type 2 diabetes mellitus (T2DM) and albuminuria were treated with dapagliflozin and placebo for 12 weeks (10 mg/day, n=36). ELISA was used to determine concentrations of collectin kidney 1 (CL-K1), collectin liver 1 (CL-L1), mannose-binding lectin (MBL), MBL-associated serine protease 2 (MASP-2), the anaphylatoxin complement factor 3a (C3a), the stable C3 split product C3dg and the membrane attack complex (sC5b-9). As published before, dapagliflozin treatment lowered Hba In patients with type 2 diabetes and albuminuria, SGLT-2 inhibition resulted in modest C3 activation in plasma, likely not driven by primary changes in circulating collectins and not resulting in changes in membrane attack complex. Based on systemic analyses, organ-specific local protective effects of gliflozins against complement activation cannot be excluded.

Sections du résumé

BACKGROUND BACKGROUND
Sodium-glucose cotransporter 2 (SGLT- 2) inhibitors exert cardiovascular and kidney-protective effects in people with diabetes. Attenuation of inflammation could be important for systemic protection. The lectin pathway of complement system activation is linked to diabetic nephropathy. We hypothesized that SGLT-2 inhibitors lower the circulating level of pattern-recognition molecules of the lectin cascade and attenuate systemic complement activation.
METHODS METHODS
Analysis of paired plasma samples from the DapKid crossover intervention study where patients with type 2 diabetes mellitus (T2DM) and albuminuria were treated with dapagliflozin and placebo for 12 weeks (10 mg/day, n=36). ELISA was used to determine concentrations of collectin kidney 1 (CL-K1), collectin liver 1 (CL-L1), mannose-binding lectin (MBL), MBL-associated serine protease 2 (MASP-2), the anaphylatoxin complement factor 3a (C3a), the stable C3 split product C3dg and the membrane attack complex (sC5b-9).
RESULTS RESULTS
As published before, dapagliflozin treatment lowered Hba
CONCLUSION CONCLUSIONS
In patients with type 2 diabetes and albuminuria, SGLT-2 inhibition resulted in modest C3 activation in plasma, likely not driven by primary changes in circulating collectins and not resulting in changes in membrane attack complex. Based on systemic analyses, organ-specific local protective effects of gliflozins against complement activation cannot be excluded.

Identifiants

pubmed: 38518448
pii: S0171-2985(24)00015-9
doi: 10.1016/j.imbio.2024.152797
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

152797

Informations de copyright

Copyright © 2024. Published by Elsevier GmbH.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Mia Jensen (M)

Unit of Cardiovascular and Renal Research, Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark. Electronic address: Miajensen@health.sdu.dk.

Mie K Eickhoff (MK)

Steno Diabetes Center Copenhagen, Herlev, Denmark.

Frederik Persson (F)

Steno Diabetes Center Copenhagen, Herlev, Denmark.

Peter Rossing (P)

Steno Diabetes Center Copenhagen, Herlev, Denmark; University of Copenhagen, Department of Clinical Medicine, Copenhagen, Denmark.

Steffen Thiel (S)

Department of Biomedicine, Aarhus University, Aarhus, Denmark.

Søren W K Hansen (SWK)

Unit for Cancer and Inflammation Research, Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark.

Yaseelan Palarasah (Y)

Unit for Cancer and Inflammation Research, Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark.

Per Svenningsen (P)

Unit of Cardiovascular and Renal Research, Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark.

Boye L Jensen (BL)

Unit of Cardiovascular and Renal Research, Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark.

Classifications MeSH