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.
Highlights
Intracerebral hemorrhage (ICH) is frequently accompanied by infection ranging from 11 to 31% and long-term functional impairment (Ali et al, 2009; Lord et al, 2014)
We focus on the crosstalk between intracerebral hemorrhage (ICH) and sepsis and attempt to identify the mechanism of cerebral dysfunction, aiming to provide a unique and systematic insight into the interaction of the two diseases and guide indications for clinical treatment
Under the mediation of systemic inflammation and circulatory dysfunction, the pathological changes can be observed in multiple organs of the patients with ICH or sepsis
Summary
Intracerebral hemorrhage (ICH) is frequently accompanied by infection ranging from 11 to 31% and long-term functional impairment (Ali et al, 2009; Lord et al, 2014). The peripheral immune cells are selected and activated by invasive bacteria or toxins in circulation, secreting a series of inflammatory cytokines to induce the systemic inflammatory responses, which further amplify cerebral cell signal cascades (Singer et al, 2018) and bring catastrophic damage to the central nervous system (CNS).
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