Skip to main content
Journal cover image

Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion.

Publication ,  Journal Article
Sanchez, S; Chimenti, MS; Lu, Y; Sagues, E; Gudino, A; Dier, C; Hasan, D; Samaniego, EA
Published in: Transl Stroke Res
February 2025

Emerging evidence indicates that aneurysmal subarachnoid hemorrhage (aSAH) elicits a response from both innate and adaptive immune systems. An upregulation of CD8 + CD161 + cells has been observed in the cerebrospinal fluid (CSF) after aSAH, yet the precise role of these cells in the context of aSAH is unkown. CSF samples from patients with aSAH and non-aneurysmal SAH (naSAH) were analyzed. Single-cell RNA sequencing (scRNAseq) was performed on CD8 + CD161 + sorted samples from aSAH patients. Cell populations were identified using "clustering." Gene expression levels of ten previously described genes involved in inflammation were quantified from aSAH and naSAH samples using RT-qPCR. The study focused on the following genes: CCL5, CCL7, APOE, SPP1, CXCL8, CXCL10, HMOX1, LTB, MAL, and HLA-DRB1. Gene clustering analysis revealed that monocytes, NK cells, and T cells expressed CD8 + CD161 + in the CSF of patients with aSAH. In comparison to naSAH samples, aSAH samples exhibited higher mRNA levels of CXCL10 (median, IQR = 90, 16-149 vs. 0.5, 0-6.75, p = 0.02). A trend towards higher HMOX1 levels was also observed in aSAH (median, IQR = 12.6, 9-17.6 vs. 2.55, 1.68-5.7, p = 0.076). Specifically, CXCL10 and HMOX1 were expressed by the monocyte subpopulation. Monocytes, NK cells, and T cells can potentially express CD8 + CD161 + in patients with aSAH. Notably, monocytes show high levels of CXCL10. The elevated expression of CXCL10 in aSAH compared to naSAH indicates its potential significance as a target for future studies.

Duke Scholars

Published In

Transl Stroke Res

DOI

EISSN

1868-601X

Publication Date

February 2025

Volume

16

Issue

1

Start / End Page

88 / 95

Location

United States

Related Subject Headings

  • Subarachnoid Hemorrhage
  • Monocytes
  • Middle Aged
  • Male
  • Humans
  • Female
  • Chemokine CXCL10
  • Aged
  • Adult
  • 3209 Neurosciences
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Sanchez, S., Chimenti, M. S., Lu, Y., Sagues, E., Gudino, A., Dier, C., … Samaniego, E. A. (2025). Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion. Transl Stroke Res, 16(1), 88–95. https://doi.org/10.1007/s12975-024-01259-4
Sanchez, Sebastian, Michael S. Chimenti, Yongjun Lu, Elena Sagues, Andres Gudino, Carlos Dier, David Hasan, and Edgar A. Samaniego. “Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion.Transl Stroke Res 16, no. 1 (February 2025): 88–95. https://doi.org/10.1007/s12975-024-01259-4.
Sanchez S, Chimenti MS, Lu Y, Sagues E, Gudino A, Dier C, et al. Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion. Transl Stroke Res. 2025 Feb;16(1):88–95.
Sanchez, Sebastian, et al. “Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion.Transl Stroke Res, vol. 16, no. 1, Feb. 2025, pp. 88–95. Pubmed, doi:10.1007/s12975-024-01259-4.
Sanchez S, Chimenti MS, Lu Y, Sagues E, Gudino A, Dier C, Hasan D, Samaniego EA. Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion. Transl Stroke Res. 2025 Feb;16(1):88–95.
Journal cover image

Published In

Transl Stroke Res

DOI

EISSN

1868-601X

Publication Date

February 2025

Volume

16

Issue

1

Start / End Page

88 / 95

Location

United States

Related Subject Headings

  • Subarachnoid Hemorrhage
  • Monocytes
  • Middle Aged
  • Male
  • Humans
  • Female
  • Chemokine CXCL10
  • Aged
  • Adult
  • 3209 Neurosciences