Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion.
Sebastian SanchezMichael S ChimentiYongjun LuElena SaguesAndres GudinoCarlos DierDavid HasanEdgar A SamaniegoPublished in: Translational stroke research (2024)
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.
Keyphrases
- single cell
- gene expression
- rna seq
- nk cells
- dendritic cells
- cerebrospinal fluid
- induced apoptosis
- peripheral blood
- poor prognosis
- end stage renal disease
- newly diagnosed
- chronic kidney disease
- oxidative stress
- high throughput
- cell proliferation
- immune response
- stem cells
- climate change
- prognostic factors
- signaling pathway
- skeletal muscle
- mesenchymal stem cells
- high fat diet
- adipose tissue
- intensive care unit
- binding protein
- endothelial cells
- acute respiratory distress syndrome
- cell death
- hepatitis b virus
- cell therapy
- data analysis
- respiratory failure
- extracorporeal membrane oxygenation
- genome wide identification