gms | German Medical Science

70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

12.05. - 15.05.2019, Würzburg

Immunophenotyping of intrathecal inflammatory response in aneurysmatic subarachnoid haemorrhage reveals distinct monocytic activation and chemokine patterns

Immunphänotypisierung der intrathekalen Inflammation bei aneurysmatischer subarachnoidaler Blutung zeigt distinkte Monozytenaktivierung und Chemokine-Produktion

Meeting Abstract

  • presenting/speaker Malte Mohme - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland
  • Thomas Sauvigny - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland
  • Marius Mader - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland
  • Nils Schweingruber - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurologie, Hamburg, Deutschland
  • Jan Regelsberger - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland
  • Nils Ole Schmidt - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland
  • Manfred Westphal - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland
  • Katrin Lamszus - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland
  • Eva Tolosa - Universitätsklinikum Hamburg-Eppendorf, Institut für Immunologie, Hamburg, Deutschland
  • Patrick Czorlich - Universitätsklinikum Hamburg-Eppendorf, Klinik für Neurochirurgie, Hamburg, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie. Würzburg, 12.-15.05.2019. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocV216

doi: 10.3205/19dgnc233, urn:nbn:de:0183-19dgnc2336

Published: May 8, 2019

© 2019 Mohme et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Objective: The pathophysiology of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) is still incompletely understood. Intrathecal inflammatory immune activation is suspected to play a major role for the induction of vasospasm and DCI. The aim of this study is to identify immune cell subsets and inflammatory mediators involved in the pathogenesis of DCI.

Methods: We prospectively collected blood and cerebrospinal fluid (CSF) from 25 patients with aneurysmal subarachnoid hemorrhage at an early and a late time points. Fifteen immune cell subsets were analyzed using a multicolor antibody panel and flow cytometry. In addition, 26 chemokines and T helper cell cytokines were assessed using a bead-based immunofluorescence assay. Statistical testing and correlative analysis were performed for Hunt & Hess grading, overall outcome and prevalence of DCI.

Results: Our results demonstrate an intrathecal immune activation with increased prevalence of conventional CD4 T cells (CD4+ CD25+), as well as expression of the CD163 scavenger receptor on monocytes. The inflammatory response was also reflected in increased IFNy production (p<0.05), CD11c+ infiltration and prevalence of plasmacytoid dendritic cells (pDC). Initially present CD14dim activated monocytes converted to classical CD14- CD16+ monocytes throughout the disease course. The intrathecal chemokine response was represented by IP-10, MIG, I-TAC and GROa (p=0.05–0.0001), chemoattractants contributing to the recruitment of additional immune cells to the site of inflammation. Statistical analysis shows strong correlation of distinct patterns to the prevalence of DCI and outcome.

Conclusion: We demonstrate that monocytes and T cells are activated intrathecally during aSAH and mediate a local inflammatory response which is presumably driven by interferons and the subsequent chemokine cascade. Our data shows that the distinct pattern of immune activation correlates to the prevalence of DCI, indicating a pathophysiological connection to the incidence of vasospasm.