Sepsis-Exacerbated Brain Dysfunction After Intracerebral Hemorrhage
Open Access
- 21 January 2022
- journal article
- review article
- Published by Frontiers Media SA in Frontiers in Cellular Neuroscience
- Vol. 15, 819182
- https://doi.org/10.3389/fncel.2021.819182
Abstract
Sepsis susceptibility is significantly increased in patients with intracerebral hemorrhage (ICH), owing to immunosuppression and intestinal microbiota dysbiosis. To date, ICH with sepsis occurrence is still difficult for clinicians to deal with, and the mortality, as well as long-term cognitive disability, is still increasing. Actually, intracerebral hemorrhage and sepsis are mutually exacerbated via similar pathophysiological mechanisms, mainly consisting of systemic inflammation and circulatory dysfunction. The main consequence of these two processes is neural dysfunction and multiple organ damages, notably, via oxidative stress and neurotoxic mediation under the mediation of central nervous system activation and blood-brain barrier disruption. Besides, the comorbidity-induced multiple organ damages will produce numerous damage-associated molecular patterns and consequently exacerbate the severity of the disease. At present, the prospective views are about operating artificial restriction for the peripheral immune system and achieving cross-tolerance among organs via altering immune cell composition to reduce inflammatory damage.This publication has 126 references indexed in Scilit:
- Toll‐like receptor 4 contributes to poor outcome after intracerebral hemorrhageAnnals of Neurology, 2011
- Molecular Pathophysiology of Cerebral HemorrhageStroke, 2011
- Toll-Like Receptor Signaling Pathways—Therapeutic OpportunitiesMediators of Inflammation, 2010
- HMBG1 Mediates Ischemia—Reperfusion Injury by TRIF-Adaptor Independent Toll-Like Receptor 4 SignalingJournal of Cerebral Blood Flow & Metabolism, 2010
- Pattern Recognition Receptors and InflammationCell, 2010
- Elevation of High-Mobility Group Protein Box-1 in Serum Correlates with Severity of Acute Intracerebral HemorrhageMediators of Inflammation, 2010
- Sepsis-Associated Encephalopathy: A Magnetic Resonance Imaging and Spectroscopy StudyJournal of Cerebral Blood Flow & Metabolism, 2009
- Blockade of adrenoreceptors inhibits the splenic response to strokeExperimental Neurology, 2009
- Role of endothelial nitric oxide synthase-derived nitric oxide in activation and dysfunction of cerebrovascular endothelial cells during early onsets of sepsisAmerican Journal of Physiology-Heart and Circulatory Physiology, 2008
- Bid-induced release of AIF from mitochondria causes immediate neuronal cell deathCell Death & Differentiation, 2008