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Published on: September 25, 2019
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Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack
Christopher W L Armstrong1, Erika Bosio2, Claire Neil2
1Dept. of Emergency Medicine, Royal Perth Hospital, Perth, WA, Australia.
Summary
Stroke patients show distinct immune responses. Ischaemic stroke involves reduced Granzyme B (GzmB) and increased MMP-9 and S100A12, indicating innate immune system involvement and potential therapeutic targets.
Area of Science:
- Neuroimmunology
- Stroke Pathophysiology
- Biomarker Discovery
Background:
- Previous case study identified Granzyme B (GzmB), S100A12, and MMP-9 changes in early stroke.
- Understanding early immune responses in stroke is crucial for managing secondary injury.
Purpose of the Study:
- To investigate GzmB, S100A12, and MMP-9 in patients with suspected stroke within 6 hours of symptom onset.
- To differentiate immune profiles between ischaemic stroke, haemorrhagic stroke, transient ischaemic attack (TIA), and healthy controls.
Main Methods:
- Blood samples collected at multiple time points (0, 1, 3, 24 hours) post-enrolment.
- Analysis included cellular populations (CD8+, CD8-, NK cells), protein levels (GzmB, S100A12, MMP-9), and gene expression.
- Patient groups: ischaemic stroke (n=18), haemorrhagic stroke (n=11), TIA (n=9), and healthy controls (n=10).
Main Results:
- Increased intracellular GzmB observed in all cell types across stroke groups.
- Ischaemic stroke patients showed reduced GzmB gene expression, elevated MMP-9 and S100A12 compared to TIA and controls.
- Neutrophilia was prominent in infarct and haemorrhage groups; TIA patients resembled controls.
Conclusions:
- Stroke elicits a spectrum of immune responses, with TIA showing minimal changes.
- Infarct and haemorrhage involve GzmB inhibition, increased neutrophils, and associated mediators, suggesting a significant innate immune role.
- Identified biomarkers (GzmB, S100A12, MMP-9) may offer targets for reducing secondary stroke injury.

