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Published on: December 4, 2017
Immunophenotyping of cerebrospinal fluid cells in ischaemic stroke
A Schulte-Mecklenbeck1, I Kleffner2, C Beuker1
1Department of Neurology, University of Münster, Münster.
Insights
Immune cell counts in cerebrospinal fluid (CSF) show minimal changes after ischaemic stroke, indicating CSF is not a reliable biomarker for brain inflammation or guiding immune therapies.
Area of Science:
- Neuroscience
- Immunology
- Stroke Research
Background:
- Immune cell infiltration into the brain post-ischaemic stroke contributes to neuronal damage.
- Cerebrospinal fluid (CSF) is accessible and may reflect brain inflammation.
- Limited studies exist on CSF immune cells in human stroke patients.
Purpose of the Study:
- To conduct extensive immune-cell profiling in CSF and peripheral blood of acute ischaemic stroke patients.
- To compare CSF immune cell profiles between stroke patients and healthy controls.
- To investigate associations between CSF immune cells, infarct size, and time from symptom onset.
Main Methods:
- Retrospective cohort study design.
- Immune-cell profiling of CSF and peripheral blood.
- Quantification of infarct size on follow-up imaging.
Main Results:
- 90 ischaemic stroke patients and 22 controls were analyzed.
- CSF total protein was elevated post-stroke (P=0.008).
- CSF white blood cell counts, and proportions of lymphocytes, monocytes, and granulocytes did not significantly differ between groups or correlate with infarct size.
Conclusions:
- Ischaemic stroke causes minimal changes in CSF immune cell counts and composition.
- CSF analysis is not a suitable biomarker for parenchymal brain inflammation in stroke.
- CSF immune cell profiling may not guide future immune therapies for stroke.
Background And Purpose:
Post-ischaemic immune cell invasion into the brain is well characterized in animal stroke models and contributes to neuronal damage. Therefore, it represents a promising therapeutic target. Cerebrospinal fluid (CSF) is easily accessible and may reflect cellular events within the parenchyma. However, comprehensive studies on CSF immune cells in patients with stroke are lacking.
Methods:
In a retrospective cohort study, we performed extensive immune-cell profiling in CSF and peripheral blood of patients with acute ischaemic stroke and healthy controls. In patients with stroke, infarct size was quantified on follow-up imaging.
Results:
Overall, 90 patients with ischaemic stroke and 22 controls were included in our study. After stroke, the total protein was increased (537.3 vs. 353.2 mg/L, P = 0.008) and the mean total white cell count was slightly but non-significantly elevated (1.76 vs. 0.50 cells/μL, P = 0.059). Proportions of CSF lymphocytes, monocytes and granulocytes and their respective subsets did not differ between patients with stroke and controls. In addition, there were no associations between proportions of major leukocyte subsets in CSF and the time from symptom onset to CSF sampling, infarct size or infarct localization.
Conclusions:
Ischaemic stroke induces only a very slight increase of CSF immune cells without changes in the composition of immune cell subsets, thus indicating that parenchymal inflammation is not sufficiently reflected in the CSF. Our findings suggest that CSF is not a major invasion route for immune cells and that CSF cell analyses are not suitable as biomarkers to guide future immune therapies for stroke.
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