Relevance of Cerebral Interleukin-6 After Aneurysmal Subarachnoid Hemorrhage

Sarrafzadeh, Asita; Schlenk, Florian; Gericke, Christine; Vajkoczy, Peter

doi:10.1007/s12028-010-9432-4

Cited by 121 publications

(107 citation statements)

References 37 publications

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“…In one sense, the degree of inflammatory responses could reflect the severity of EBI. Similar to our study, other studies also revealed that high levels of inflammatory cytokines such as IL-2, IL-6, IL-8 and CRP correlated with a higher clinical grade (4,9,11,17). The process of antiinflammation would be activated simultaneously after SAH,…”

Section: █ Resultssupporting

confidence: 89%

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Zhong

Zhang²,

Zhao³

et al. 2015

Turkish Neurosurgery

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ABSTRACTcytokines such as interleukin-6 (IL-6) and C-reactive protein (CRP) would increase early after SAH, inflammatory response would have been involved in the course of EBI. So far, most recent studies on inflammatory cytokines in SAH have focused on DCV while fewer studies have focused on EBI and its complications such as pneumonia, which influence the clinical course of aneurysmal SAH. Clinically, a serious initial clinical grade usually indicates a severe EBI after SAH (15), and infection is usually associated with immune dysfunction. █ INTRODUCTION D espite early surgical or endovascular treatment, aneurysmal subarachnoid hemorrhage (SAH) still has a high mortality and morbidity rate. Recently, early brain injury (EBI) was considered as an important determinant factor of outcome except delayed cerebral vasospasm (DCV) after aneurysmal SAH (6,19). The exact mechanism of EBI has still not been clearly demonstrated and the levels of inflammatory AIm: To assess the association between inflammatory response and early brain injury (EBI), and the association between inflammatory response and the following pneumonia after aneurysmal subarachnoid hemorrhage (SAH). mATERIAl and mEThODS: Eighty-nine patients with spontaneous SAH and 12 patients with unruptured aneurysm were included in this prospective study. The systemic inflammatory biomarkers such as C-reactive protein (CRP), IL-1β, IL-2,IL-6,IL-8, IL10 and T leukocyte subsets were measured within 24 hours after admission. Their clinical features and laboratory findings were clearly reviewed and univariate analysis was used to find the main predictors. RESUlTS:The levels of serum inflammatory cytokines especially IL-6 (p=0.004) and CRP (p=0.014) would significantly increase after aneurysm SAH. Higher Fisher grades on admission result in higher levels of IL-6 and IL-10 (pIL-6=0.003. pIL-10=0.002), and higher levels of IL-6, IL-10 and CRP were significantly associated with severe EBI, and increased the susceptibility to pneumonia (p<0.05). The counts of CD3+ T Cells would decrease after aneurysm rupture (p=0.001), especially in patients with a poor initial clinical grade. A reversed correlation between IL-6 level and CD3 T cells count was revealed in this study (p=0.014,r=-0.249); a lower CD4 T-Cells counts might lead to subsequent pneumonia after SAH (p=0.041). The levels of serum inflammatory cytokines were not different between aneurysmal and non-aneurysmal SAH.CONClUSION: Systemic inflammatory response would be activated after aneurysm rupture; a similar systemic inflammatory response would be noticed in non-aneurysmal SAH. The degree of inflammatory response could reflect the severity of EBI, and excessive inflammatory response could also aggravate EBI, induce immunodepression and increase the susceptibility to infections. Inflammatory cytokines such as IL-6, IL-10 and CRP are important predictors.

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Section: █ Resultssupporting

confidence: 89%

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Zhong

Zhang²,

Zhao³

et al. 2015

Turkish Neurosurgery

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“…Increased synthesis may be secondary to the host inflammatory response because the hemopexin promoter is interleukin-6 responsive, 11 and interleukin-6 levels are elevated in SAH CSF. 12 Decreased CD91-mediated scavenging may be because of plateauing in heme-hemopexin uptake because heme and hemopexin were detected simultaneously in the CSF. Also, because CD91 has multiple ligands, it is possible that there is competition for CD91 from other ligands, such as ApoE.…”

Section: March 2016mentioning

confidence: 99%

Heme–Hemopexin Scavenging Is Active in the Brain and Associates With Outcome After Subarachnoid Hemorrhage

Garland

Durnford

Okemefuna

et al. 2016

Stroke

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Background and Purpose— Long-term outcome after subarachnoid hemorrhage (SAH) is potentially linked to cytotoxic heme. Free heme is bound by hemopexin and rapidly scavenged by CD91. We hypothesized that heme scavenging in the brain would be associated with outcome after hemorrhage. Methods— Using cerebrospinal fluid and tissue from patients with SAH and control individuals, the activity of the intracranial CD91–hemopexin system was examined using ELISA, ultrahigh performance liquid chromatography, and immunohistochemistry. Results— In control individuals, cerebrospinal fluid hemopexin was mainly synthesized intrathecally. After SAH, cerebrospinal fluid hemopexin was high in one third of cases, and these patients had a higher probability of delayed cerebral ischemia and poorer neurological outcome. The intracranial CD91–hemopexin system was active after SAH because CD91 positively correlated with iron deposition in brain tissue. Heme–hemopexin uptake saturated rapidly after SAH because bound heme accumulated early in the cerebrospinal fluid. When the blood–brain barrier was compromised after SAH, serum hemopexin level was lower, suggesting heme transfer to the circulation for peripheral CD91 scavenging. Conclusions— The CD91–heme–hemopexin scavenging system is important after SAH and merits further study as a potential prognostic marker and therapeutic target.

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“…Some of the factors involved after ischemic stroke are tumor necrosis factor-a, interleukin-1b (IL-1b), IL-6, and inducible nitric oxide synthase, which are produced by a variety of activated cell types; endothelial cells, microglia, neurons, platelets, monocytes, macrophages, and fibroblasts (Huang et al, 2006). Furthermore, there is now clinical evidence of an upregulation of IL-6 after SAH (Sarrafzadeh et al, 2011).…”

Section: The Role Of Inflammation In Cerebrovascular Pathophysiology mentioning

confidence: 99%

Vascular plasticity in cerebrovascular disorders

Edvinsson

Povlsen

2011

J Cereb Blood Flow Metab

115

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Cerebral ischemia remains a major cause of morbidity and mortality with little advancement in subacute treatment options. This review aims to cover and discuss novel insight obtained during the last decade into plastic changes in the vasoconstrictor receptor profiles of cerebral arteries and microvessels that takes place after different types of stroke. Receptors like the endothelin type B, angiotensin type 1, and 5-hydroxytryptamine type 1B/1D receptors are upregulated in the smooth muscle layer of cerebral arteries after different types of ischemic stroke as well as after subarachnoid hemorrhage, yielding rather dramatic changes in the contractility of the vessels. Some of the signal transduction processes mediating this receptor upregulation have been elucidated. In particular the extracellular regulated kinase 1/2 pathway, which is activated early in the process, has proven to be a promising therapeutic target for prevention of vasoconstrictor receptor upregulation after stroke. Together, those findings provide new perspectives on the pathophysiology of ischemic stroke and point toward a novel way of reducing vasoconstriction, neuronal cell death, and thus neurologic deficits after stroke.

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Relevance of Cerebral Interleukin-6 After Aneurysmal Subarachnoid Hemorrhage

Cited by 121 publications

References 37 publications

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Heme–Hemopexin Scavenging Is Active in the Brain and Associates With Outcome After Subarachnoid Hemorrhage

Vascular plasticity in cerebrovascular disorders

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