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Peer-reviewedCC BY-NC-NDJournal of the American Heart Association

Temporal Dynamics of Complement Activation and Outcome in Patients With Acute Ischemic Stroke

  • Yan Wang1,2
  • Willeke F. Westendorp1,2
  • Merijn W. Bijlsma2,1
  • Michael W. T. Tanck1
  • Wing Kit Man1,2
  • Matthijs C. Brouwer1,2
  • Inge A. Mulder2,3,4
  • Jonathan M. Coutinho1,2,4
  • Diederik van de Beek1,2
4 affiliations
  1. 1Amsterdam University Medical Center
  2. 2Amsterdam Neuroscience
  3. 3Amsterdam University Medical Center Amsterdam
  4. 4Amsterdam Cardiovascular Sciences
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Abstract

BACKGROUND: Immune-mediated inflammatory responses exacerbate brain injury and affect the prognosis in acute ischemic stroke. METHODS: We characterized longitudinal complement activation after acute ischemic stroke using serial plasma samples from 10 patients and 8 controls. Initial markers of classical (C1q), lectin (mannose-binding lectin), and alternative (complement factor Bb) pathways, as well as regulatory (complement factor H) and downstream markers (C3a, C5a, and C5b-9) were measured by ELISA at 9 time points. RESULTS: Patients with stroke showed broad complement activation, with increased C1q, mannose-binding lectin, complement factor Bb, C3a, C5a, and C5b-9, and reduced complement factor H compared with controls. Complement components showed distinct temporal patterns during follow-up. Complement factor Bb levels were lower in patients with unfavorable functional outcome and in those with moderate-to-severe stroke. C1q and C3a trajectories differed according to functional outcome, whereas C3a trajectories also differed according to stroke severity. C1q trajectories differed according to age group and infarct volume. CONCLUSIONS: These findings suggest dynamic, pathway-specific complement activation after acute ischemic stroke and highlight the need for larger studies to clarify its prognostic and therapeutic relevance.

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Cite

BibTeXRIS
BibTeX
@article{wang2026temporal,
  title = {{Temporal Dynamics of Complement Activation and Outcome in Patients With Acute Ischemic Stroke}},
  author = {Yan Wang and Willeke F. Westendorp and Merijn W. Bijlsma and Michael W. T. Tanck and Wing Kit Man and Matthijs C. Brouwer and Inge A. Mulder and Jonathan M. Coutinho and Diederik van de Beek},
  journal = {Journal of the American Heart Association},
  year = {2026},
  month = oct,
  doi = {10.1161/jaha.125.048042},
  url = {https://www.ahajournals.org/doi/10.1161/JAHA.125.048042},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Temporal Dynamics of Complement Activation and Outcome in Patients With Acute Ischemic Stroke
AU  - Yan Wang
AU  - Willeke F. Westendorp
AU  - Merijn W. Bijlsma
AU  - Michael W. T. Tanck
AU  - Wing Kit Man
AU  - Matthijs C. Brouwer
AU  - Inge A. Mulder
AU  - Jonathan M. Coutinho
AU  - Diederik van de Beek
PY  - 2026
DA  - 2026/10/20
JO  - Journal of the American Heart Association
DO  - 10.1161/jaha.125.048042
UR  - https://www.ahajournals.org/doi/10.1161/JAHA.125.048042
AB  - BACKGROUND: Immune-mediated inflammatory responses exacerbate brain injury and affect the prognosis in acute ischemic stroke. METHODS: We characterized longitudinal complement activation after acute ischemic stroke using serial plasma samples from 10 patients and 8 controls. Initial markers of classical (C1q), lectin (mannose-binding lectin), and alternative (complement factor Bb) pathways, as well as regulatory (complement factor H) and downstream markers (C3a, C5a, and C5b-9) were measured by ELISA at 9 time points. RESULTS: Patients with stroke showed broad complement activation, with increased C1q, mannose-binding lectin, complement factor Bb, C3a, C5a, and C5b-9, and reduced complement factor H compared with controls. Complement components showed distinct temporal patterns during follow-up. Complement factor Bb levels were lower in patients with unfavorable functional outcome and in those with moderate-to-severe stroke. C1q and C3a trajectories differed according to functional outcome, whereas C3a trajectories also differed according to stroke severity. C1q trajectories differed according to age group and infarct volume. CONCLUSIONS: These findings suggest dynamic, pathway-specific complement activation after acute ischemic stroke and highlight the need for larger studies to clarify its prognostic and therapeutic relevance.
SN  - 2047-9980
ER  -