White blood cell subtypes and neutrophil extracellular traps content as biomarkers for stroke etiology in acute ischemic stroke clots retrieved by mechanical thrombectomy.

Etiology Ischemic stroke Lymphocytes Macrophages Neutrophil extracellular traps Neutrophils White blood cells

Journal

Thrombosis research
ISSN: 1879-2472
Titre abrégé: Thromb Res
Pays: United States
ID NLM: 0326377

Informations de publication

Date de publication:
15 Dec 2023
Historique:
received: 01 09 2023
revised: 17 11 2023
accepted: 12 12 2023
medline: 19 12 2023
pubmed: 19 12 2023
entrez: 19 12 2023
Statut: aheadofprint

Résumé

Lymphocytes, macrophages, neutrophils, and neutrophil extracellular traps (NETs) associate with stroke risk factors and form a thrombus through different mechanisms. We investigated the total WBCs, WBC subtypes and NETs composition in acute ischemic stroke (AIS) clots to identify possible etiological differences that could help us further understand the process of thrombosis that leads to AIS. AIS clots from 100 cases each of atherothrombotic (AT), cardioembolic (CE) and cryptogenic stroke etiology were collected per-pass as part of the CÚRAM RESTORE registry of AIS clots. Martius Scarlet Blue stain was used to identify the main histological components of the clots. Immunohistochemical staining was used to identify neutrophils, lymphocytes, macrophages, and NETs patterns. The cellular and histological components were quantified using Orbit Image Analysis software. AT clots were larger, with more red blood cells and fewer WBCs than CE clots. AT clots had more lymphocytes and cryptogenic clots had fewer macrophages than other etiologies. Most significantly, CE clots showed higher expression of neutrophils and extracellular web-like NETs compared to AT and cryptogenic clots. There was also a significantly higher distribution of web-like NETs around the periphery of the CE clots while a mixed distribution was observed in AT clots. The difference in neutrophil and NETs expression in clots from different etiologies may provide insight into the mechanism of clot formation.

Sections du résumé

BACKGROUND BACKGROUND
Lymphocytes, macrophages, neutrophils, and neutrophil extracellular traps (NETs) associate with stroke risk factors and form a thrombus through different mechanisms. We investigated the total WBCs, WBC subtypes and NETs composition in acute ischemic stroke (AIS) clots to identify possible etiological differences that could help us further understand the process of thrombosis that leads to AIS.
METHODS METHODS
AIS clots from 100 cases each of atherothrombotic (AT), cardioembolic (CE) and cryptogenic stroke etiology were collected per-pass as part of the CÚRAM RESTORE registry of AIS clots. Martius Scarlet Blue stain was used to identify the main histological components of the clots. Immunohistochemical staining was used to identify neutrophils, lymphocytes, macrophages, and NETs patterns. The cellular and histological components were quantified using Orbit Image Analysis software.
RESULTS RESULTS
AT clots were larger, with more red blood cells and fewer WBCs than CE clots. AT clots had more lymphocytes and cryptogenic clots had fewer macrophages than other etiologies. Most significantly, CE clots showed higher expression of neutrophils and extracellular web-like NETs compared to AT and cryptogenic clots. There was also a significantly higher distribution of web-like NETs around the periphery of the CE clots while a mixed distribution was observed in AT clots.
CONCLUSION CONCLUSIONS
The difference in neutrophil and NETs expression in clots from different etiologies may provide insight into the mechanism of clot formation.

Identifiants

pubmed: 38113606
pii: S0049-3848(23)00352-3
doi: 10.1016/j.thromres.2023.12.005
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-8

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

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

Duaa Jabrah (D)

Department of Physiology, University of Galway, Galway, Ireland.

Rosanna Rossi (R)

Department of Physiology, University of Galway, Galway, Ireland; CÚRAM-SFI Centre for Research in Medical Devices, University of Galway, Galway, Ireland.

Sara Molina (S)

Department of Physiology, University of Galway, Galway, Ireland; CÚRAM-SFI Centre for Research in Medical Devices, University of Galway, Galway, Ireland.

Andrew Douglas (A)

Department of Physiology, University of Galway, Galway, Ireland.

Abhay Pandit (A)

CÚRAM-SFI Centre for Research in Medical Devices, University of Galway, Galway, Ireland.

Ray McCarthy (R)

Cerenovus, Galway Neuro Technology Centre, Galway, Ireland.

Michael Gilvarry (M)

Cerenovus, Galway Neuro Technology Centre, Galway, Ireland.

Eric Ceder (E)

Department of Interventional and Diagnostic Neuroradiology, Sahlgrenska University Hospital, Institute of Clinical Sciences, Department of Radiology, Sahlgrenska Academy at University of Gothenburg, Sweden.

Seán Fitzgerald (S)

Department of Physiology, University of Galway, Galway, Ireland.

Dennis Dunker (D)

Department of Interventional and Diagnostic Neuroradiology, Sahlgrenska University Hospital, Institute of Clinical Sciences, Department of Radiology, Sahlgrenska Academy at University of Gothenburg, Sweden.

Annika Nordanstig (A)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg and Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Petra Redfors (P)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg and Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Turgut Tatlisumak (T)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg and Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Alan O'Hare (A)

Department of Radiology, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.

Sarah Power (S)

Department of Radiology, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.

Paul Brennan (P)

Department of Radiology, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.

Peter Owens (P)

Centre for Microscopy and Imaging, University of Galway, Galway, Ireland.

András Nagy (A)

Department of Neurointerventions, National Institute of Neurosciences, Budapest, Hungary.

Ágnes Vadász (Á)

Department of Neurointerventions, National Institute of Neurosciences, Budapest, Hungary.

Simon F De Meyer (SF)

Laboratory for Thrombosis Research, KU Leuven Campus Kulak, Kortrijk, Belgium.

Georgios Tsivgoulis (G)

Second Department of Neurology, National & Kapodistrian University of Athens, "Attikon" University Hospital, Athens, Greece.

Klearchos Psychogios (K)

Metropolitan Hospital, Stroke Unit, Piraeus, Greece.

Istvan Szikora (I)

Department of Neurointerventions, National Institute of Neurosciences, Budapest, Hungary.

Katarina Jood (K)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg and Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Alexandros Rentzos (A)

Department of Interventional and Diagnostic Neuroradiology, Sahlgrenska University Hospital, Institute of Clinical Sciences, Department of Radiology, Sahlgrenska Academy at University of Gothenburg, Sweden.

John Thornton (J)

Department of Radiology, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.

Karen Doyle (K)

Department of Physiology, University of Galway, Galway, Ireland; CÚRAM-SFI Centre for Research in Medical Devices, University of Galway, Galway, Ireland. Electronic address: karen.doyle@universityofgalway.ie.

Classifications MeSH