Serum Levels of Soluble Triggering Receptor Expressed on Myeloid Cells-1 Associated with the Severity and Outcome of Acute Ischemic Stroke.
Jyun-Bin HuangNai-Ching ChenChien-Liang ChenMu-Hui FuHsiu-Yung PanChung-Yao HsuShang-Der ChenYao-Chung ChuangPublished in: Journal of clinical medicine (2020)
Stroke is a neurological emergency, where the mechanism of the blood supply to the brain is impaired, resulting in brain cell ischemia and death. Neuroinflammation is a key component in the ischemic cascade that results in cell damage and death after cerebral ischemia. The triggering receptor expressed on myeloid cells-1 (TREM-1) modulates neuroinflammation after acute ischemic stroke. In the present study, 60 patients with acute ischemic stroke, who had been subjected to neurological examinations and National Institutes of Health Stroke Scale (NIHSS) and brain magnetic resonance imaging studies, were enrolled in the emergency room of Kaohsiung Chang Gung Memorial Hospital. Twenty-four healthy volunteers were recruited as controls. The serum levels of soluble TREM-1 (sTREM-1), human S100 calcium-binding protein B (S100B), and proinflammatory cytokines and chemokines, including tumor necrosis α (TNF-α), interleukin 1β, interleukin 6 (IL-6), interleukin 8, and interferon-γ were measured immediately after acute ischemic stroke. The serum levels of sTREM-1, TNFα, IL-6, and S100B were correlated with the stroke volume and NIHSS, after acute ischemic stroke. Additionally, the serum levels of sTREM-1 were significantly positively correlated with S100B. The functional outcomes were evaluated 6 months after ischemic stroke by the Barthel index, which was correlated with the age and levels of sTREM-1 and S100B. We suggest that acute ischemic stroke induces neuroinflammation by the activation of the TREM-1 signaling pathway and the downstream inflammatory machinery that modulates the inflammatory response and ischemic neuronal cell death. From a translational perspective, our results may allow for the development of a new therapeutic strategy for acute ischemic stroke by targeting the TREM-1 signaling pathway.
Keyphrases
- acute ischemic stroke
- cerebral ischemia
- subarachnoid hemorrhage
- blood brain barrier
- brain injury
- induced apoptosis
- signaling pathway
- magnetic resonance imaging
- cell death
- healthcare
- cell cycle arrest
- inflammatory response
- public health
- binding protein
- emergency department
- atrial fibrillation
- dendritic cells
- rheumatoid arthritis
- endothelial cells
- oxidative stress
- pi k akt
- single cell
- acute myeloid leukemia
- bone marrow
- stem cells
- traumatic brain injury
- risk assessment
- endoplasmic reticulum stress
- epithelial mesenchymal transition
- lipopolysaccharide induced
- multiple sclerosis
- mesenchymal stem cells
- immune response
- lps induced
- contrast enhanced
- cell proliferation
- electronic health record
- case control