Levels of Interleukin-1β, Interleukin-18, and Tumor Necrosis Factor-α in Cerebrospinal Fluid of Aneurysmal Subarachnoid Hemorrhage Patients May Be Predictors of Early Brain Injury and Clinical Prognosis

Lv, Shengyin; Wu, Qi; Liu, Jingpeng; Shao, Jiang; Wen, Li-Li; Xue, Jingyi; Zhang, Xiangsheng; Zhang, Qingrong; Xin, Zhang

doi:10.1016/j.wneu.2017.12.076

Cited by 32 publications

(26 citation statements)

References 47 publications

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“…[36,39] IL-18, a strong proinflammatory cytokine involved in the synthesis of inflammatory mediators, has recently been shown to be a predictor of early brain injury and clinical prognosis in SAH patients as elevated concentrations correlated to cerebral edema and acute hydrocephalus. [20] It should be noted that the observed temporal pattern of IL-18 in that study differed from our study as we demonstrated a late peak of this cytokine. Urokinase (or uPA) is a serum protease that activates plasminogen to plasmin which in turn leads to thrombolysis and tissue degradation.…”

Section: Group Bcontrasting

confidence: 90%

“…[32] On the other hand, there is scarce or non-existing literature on many other proteins, some of which showed interesting temporal patterns and statistically significant peaks and trends, such as LIF, CCL11, CCL28, 4E-BP1, CD40, CXCL6, CXCL9, and IL-18. [20,[33][34][35][36] Group A Nine biomarkers showed higher day 1 values and decreasing trends throughout the observation period (Tables 3 and 4). Four of them (CCL11, LIF, MIP-1β and TRAIL) showed statistically significant early peaks with day 1 > day 4 levels but no statistically significant decreasing trends were observed.…”

Section: Discussionmentioning

confidence: 99%

“…[11][12][13] Many clinical and experimental studies report levels of single or few inflammatory biomarkers (such as cytokines) in the peripheral blood, cerebrospinal fluid (CSF) and cerebral extracellular fluid through microdialysis (MD) in SAH patients or animal models and further correlate these biomarkers with clinical parameters and outcome. [14][15][16][17][18][19][20][21][22] Although this strategy provides useful insight in the interplay between inflammation and the disease course it fails to account for the complexity of the involved mechanisms that cannot be adequately described by a single (or few) parameter(s) alone.…”

Section: Introductionmentioning

confidence: 99%

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Temporal patterns of inflammatory biomarkers measured in the cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage using multiplex Proximity Extension Assay technology.

Vlachogiannis¹,

Hillered²,

Enblad³

et al. 2020

Preprint

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Background Neuroinflammation has been extensively studied in the context of subarachnoid hemorrhage (SAH) in recent years. A common approach is correlation of levels of single or few inflammatory biomarkers with clinical parameters such as cerebral vasospasm and outcome. However, the complexity of the inflammatory response post SAH may require a more comprehensive overall approach by analyzing multiple biomarkers simultaneously. Methods Twenty-nine patients with SAH requiring insertion of external ventricular drainage were enrolled and ventricular cerebrospinal fluid was collected at days 1, 4 and 10 after hemorrhage. The levels of 92 inflammatory biomarkers were simultaneously measured in the samples using Proseek Multiplex Inflammation 1® assay (Olink Proteomics, Uppsala, Sweden) based on Proximity Extension Assay (PEA) technology. Thirty-eight proteins were excluded from further analysis due to lack of >10% of measurable values. Temporal patterns for each of the remaining 54 proteins were illustrated on graphs with medians and quartiles. Wilcoxon matched pairs test was used for comparison of the medians between time points. Results Four different patterns were visually observed with an early peak and gradually decreasing trend (9 proteins), middle peak (14 proteins), late peak after a gradually increasing trend (27 proteins) and no specific pattern (4 proteins). Several biomarkers showed statistically significant increasing trends (defined as day 1 < day 4 < day 10 values) and late peaks (day 4 < day 10), such as chemokines CXCL6 and CCL23, or significant early peaks (that is, day 1 > day 4) such as leukemia inhibitor factor (LIF) and macrophage inflammatory factor-1β (MIP-1β). No statistically significant decreasing trends (defined as day 1 > day 4 > day 10) were observed. Two proteins showed statistically significant middle peaks (chemokine CCL28 and Delta and Notch epidermal growth factor-related receptor-DNER). Conclusion The comprehensive data set provided in this study may act as an illustration of an inflammatory profile of the acute phase of SAH showing groups of biomarkers with similar temporal patterns of activation. Further studies can be designed based on these data in order to explore potential implications on early and late clinical events in the disease course.

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Section: Group Bcontrasting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Temporal patterns of inflammatory biomarkers measured in the cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage using multiplex Proximity Extension Assay technology.

Vlachogiannis¹,

Hillered²,

Enblad³

et al. 2020

Preprint

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“…A growing body of evidence has shown that EBI after SAH is closely associated with a robust inflammatory response in the cerebral cortex (2,4,50). Early increases in inflammatory cytokine production in cerebrospinal fluid and serum independently predict poor outcome in patients with SAH (50,51). Importantly, several experimental studies have offered evidence that suppression of neuroinflammation in the brain by anti-inflammatory therapy confers marked protection against EBI after SAH (17,52,53).…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin mitigates subarachnoid hemorrhage injury primarily by increasing sirtuin 1 and inhibiting the Toll‐like receptor 4 signaling pathway

Zhang

et al. 2018

The FASEB Journal

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Inflammation plays a key role in the progression of subarachnoid hemorrhage (SAH). Here, we examined the effects of astaxanthin (ATX) on the inflammatory response and secondary damage after SAH and the underlying mechanisms of action. In vivo, a prechiasmatic cistern injection model was established in rats and mice. In addition, neuron-microglia cocultures were exposed to oxyhemoglobin to mimic SAH in vitro. Western blotting revealed that protein expression of TLR4 was markedly increased in microglia at 24 h after SAH, with consequent increases in the downstream molecules myeloid differentiation factor 88 and NF-кB. Treatment with ATX significantly inhibited the TLR4 activation, increased sirtuin 1 expression, and inhibited the subsequent inflammatory response both in vivo and in vitro. ATX also significantly decreased high-mobility group box 1 nuclear translocation and secretion in neurons, an effect that was reversed by the sirtuin 1-specific inhibitor sirtinol. ATX administered 4 h after SAH ameliorated cerebral inflammation, brain edema, and neuronal death and improved neurologic function. ATX reduced neuronal death but did not improve neurologic function in TLR4 knockout mice. These results suggest that ATX reduces the proinflammatory response and secondary brain injury after SAH, primarily by increasing sirtuin 1 levels and inhibiting the TLR4 signaling pathway.-Zhang, X., Lu, Y., Wu, Q., Dai, H., Li, W., Lv, S., Zhou, X., Zhang, X., Hang, C., Wang, J. Astaxanthin mitigates subarachnoid hemorrhage injury primarily by increasing sirtuin 1 and inhibiting the Toll-like receptor 4 signaling pathway.

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“…Results from real-time PCR, western blot assay, immunohistochemistry and ELISA in SAH models showed that TLR4/NF-xo3BA signalling pathway was activated in early SAH, triggered inflammation and promoted CVS, and inhibition of TLR4/NF-xo3BA signalling pathway alleviated the degree of CVS [29]. The TLR4/NF-kB signalling pathway played an important role in the pathological process of SAH with CVS; targeted control of inflammatory factors expression effectively alleviated the occurrence of CVS secondary to SAH, thereby remarkably improving the prognosis of patients [30].…”

Section: Western Blotting Analysismentioning

confidence: 95%

Gene expression profiles and related immune-inflammatory factors in the cerebral arteries in mouse models of subarachnoid haemorrhage

Wang

Han

Wang

et al. 2020

Biotechnology & Biotechnological Equipment

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The study aimed to identify key genes involved in cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH). GSE46696 of basilar arteries of SAH mice and normal controls were downloaded from the Gene Expression Omnibus (GEO). Integrated microarray analysis was performed to identify differentially expressed genes (DEGs). GO and KEGG pathway enrichment analyses of DEGs were performed with ClueGO. The protein-protein interaction (PPI) networks were constructed using Cytoscape software. A total of 4103 DEGs were identified; among them, 254 DEGs (63 up-regulated genes and 191 down-regulated genes) showed significant differences at p < 0.05. GO analysis showed that the identified DEGs were over-represented in 16 GO terms. KEGG pathway analysis showed that pathways in immune inflammation were significantly enriched pathways for DEGs. DEGs with relatively frequent interactions after CVS secondary to SAH included MIKI,

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Levels of Interleukin-1β, Interleukin-18, and Tumor Necrosis Factor-α in Cerebrospinal Fluid of Aneurysmal Subarachnoid Hemorrhage Patients May Be Predictors of Early Brain Injury and Clinical Prognosis

Cited by 32 publications

References 47 publications

Temporal patterns of inflammatory biomarkers measured in the cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage using multiplex Proximity Extension Assay technology.

Temporal patterns of inflammatory biomarkers measured in the cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage using multiplex Proximity Extension Assay technology.

Astaxanthin mitigates subarachnoid hemorrhage injury primarily by increasing sirtuin 1 and inhibiting the Toll‐like receptor 4 signaling pathway

Gene expression profiles and related immune-inflammatory factors in the cerebral arteries in mouse models of subarachnoid haemorrhage

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