ArticleJournal of leukocyte biology2025
Temporal immune profiling in the cerebrospinal fluid and blood of patients with aneurysmal subarachnoid hemorrhage.
Article in Journal of leukocyte biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Machine Learning-Based Prediction of Delayed Cerebral Ischemia and Functional Outcome in Aneurysmal Subarachnoid Hemorrhage: The Role of CNS Infection-Related Parameters.Biomedicines · 2026Article
- Admission Inflammatory Blood Cell Ratios as Prognostic Markers of Functional Outcome After Aneurysmal Subarachnoid Hemorrhage: A Single-Center Retrospective Cohort Study.Biomedicines · 2026Article
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9 authors.
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Abstract
Delayed cerebral ischemia (DCI) is a significant complication of aneurysmal subarachnoid hemorrhage (aSAH). This study profiled immune responses after aSAH and evaluated their association with DCI onset. Twelve aSAH patients were enrolled. Leukocyte populations and cytokine levels were analyzed in cerebrospinal fluid (CSF) and peripheral blood (PB) on days 3, 5, 7, 10, and 14 post-aSAH. PB mononuclear cells (PBMCs) were collected, and their cytokine production quantified following stimulation. Mixed-effects models reveal distinct immune cell dynamics in CSF compared with blood. Monocyte/macrophage numbers continue to increase in both CSF and PBMCs for days post-aSAH. CD4+ human leukocyte antigen II+ T cells and CD8+ CD154+ T cells increased in circulation over time. Unstimulated PBMCs showed increased interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha production, peaking at 7 d post-aSAH, coinciding with typical DCI onset. Ex vivo stimulation of PBMCs showed that only IL-6 significantly changed over time. In CSF, cytokines peaked 5 d postinjury, preceding immune cell profile alterations. Our findings reveal a time-dependent immune response following aSAH, with distinct within-patient patterns in CSF and PB. The early CSF cytokine peak preceding immune cell changes suggests a potential mechanistic link and identifies the cytokine response as a potential therapeutic target. This cytokine surge may drive immune cell expansion and prime PBMCs for increased inflammatory activity, potentially contributing to DCI risk. Future studies should explore the importance and sources of specific cytokines in driving immune activation. These insights may inform the development of targeted immunomodulatory strategies for preventing or managing DCI in aSAH patients.
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