A Systematic Review of Inflammatory Cytokine Changes Following Aneurysmal Subarachnoid Hemorrhage in Animal Models and Humans

Devlin, Patrick; Ishrat, Tauheed; Stanfill, Ansley Grimes

doi:10.1007/s12975-022-01001-y

Cited by 12 publications

(7 citation statements)

References 105 publications

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“…The critical role of inflammatory states as the regulator of a plethora of diseases is widely recognized, emerging as a promising area of research for potential therapeutics. Thereby, the inflammatory mechanisms must be better understood in order to efficiently manage unregulated inflammation, improving patient outcomes following aSAH and favoring the progress for clinical translation [41]. In the current study, we provide evidence of inflammasome overactivation in aSAH patients, launching pyroptosis and leading to the release of proinflammatory cytokines and TF.…”

Section: Discussionmentioning

confidence: 63%

“…Interestingly, aSAH pathophysiology has been associated with oxidative stress and cell apoptosis, both processes related with massive DAMPs release [52,54]. So far, recent data mentioned that, after aSAH event, the red blood cells are degraded in the subarachnoid space promoting oxidative stress and activating inflammatory cascades [55,56], increasing the inflammatory cytokines [41,57,58]. Here, we propose that erythrolysis could be the triggering factor underlying NLRP3 activation in aSAH monocytes using an in vitro model.…”

Section: G F Ementioning

confidence: 71%

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NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

Nanwani-Nanwani

García-Tovar²,

Alfaro³

et al. 2022

Transl. Stroke Res.

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Aneurysmal subarachnoid hemorrhage (aSAH) is an uncommon and severe subtype of stroke leading to the loss of many years of productive life. We analyzed NLRP3 activity as well as key components of the inflammasome cascade in monocytes and plasma from 28 patients with aSAH and 14 normal controls using flow cytometry, western blot, ELISA, and qPCR technologies. Our data reveal that monocytes from patients with aSAH present an overactivation of the NLRP3 inflammasome, which results in the presence of high plasma levels of interleukin (IL)-1β, IL-18, gasdermin D, and tissue factor. Although further research is needed, we propose that serum tissue factor concentration might be a useful prognosis biomarker for clinical outcome, and for Tako-Tsubo cardiomyopathy and cerebral vasospasm prediction. Remarkably, MCC-950 inhibitor effectively blocks NLRP3 activation in aSAH monocyte culture and supresses tissue factor release to the extracellular space. Finally, our findings suggest that NLRP3 activation could be due to the release of erythrocyte breakdown products to the subarachnoid space during aSAH event. These data define NLRP3 activation in monocytes from aSAH patients, indicating systemic inflammation that results in serum TF upregulation which in turns correlates with aSAH severity and might serve as a prognosis biomarker for aSAH clinical outcome and for cerebral vasospasm and Tako-Tsubo cardiomyopathy prediction.

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Section: Discussionmentioning

confidence: 63%

Section: G F Ementioning

confidence: 71%

NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

Nanwani-Nanwani

García-Tovar²,

Alfaro³

et al. 2022

Transl. Stroke Res.

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“…Ultimately, MLKL acts on the cell membrane to form pores that lead to necroptosis by allowing the uncontrolled release of intracellular substances. 4 Oxidative Medicine and Cellular Longevity homeostasis. Caspase-12 knockout mice are insensitive to other apoptotic pathways but are significantly resistant to ER stress-induced apoptosis, indicating that caspase-12 is a specific ER stress-induced apoptosis regulator [54].…”

Section: Endoplasmic Reticulum Stress-induced Apoptosismentioning

confidence: 99%

“…Subarachnoid hemorrhage (SAH) can cause stroke and neurological damage and is often lethal [ 4 , 5 ]. Cerebral vasospasm (CVS) after SAH is the cause of many damaging effects.…”

Section: Introductionmentioning

confidence: 99%

Biological Effects and Mechanisms of Caspases in Early Brain Injury after Subarachnoid Hemorrhage

Liu

Zhou

et al. 2022

Oxidative Medicine and Cellular Longevity

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Caspases are an evolutionarily conserved family of proteases responsible for mediating and initiating cell death signals. In the past, the dysregulated activation of caspases was reported to play diverse but equally essential roles in neurodegenerative diseases, such as brain injury and neuroinflammatory diseases. A subarachnoid hemorrhage (SAH) is a traumatic event that is either immediately lethal or induces a high risk of stroke and neurological deficits. Currently, the prognosis of SAH after treatment is not ideal. Early brain injury (EBI) is considered one of the main factors contributing to the poor prognosis of SAH. The mechanisms of EBI are complex and associated with oxidative stress, neuroinflammation, blood-brain barrier disruption, and cell death. Based on mounting evidence, caspases are involved in neuronal apoptosis or death, endothelial cell apoptosis, and increased inflammatory cytokine-induced by apoptosis, pyroptosis, and necroptosis in the initial stages after SAH. Caspases can simultaneously mediate multiple death modes and regulate each other. Caspase inhibitors (including XIAP, VX-765, and Z-VAD-FMK) play an essential role in ameliorating EBI after SAH. In this review, we explore the related pathways mediated by caspases and their reciprocal regulation patterns after SAH. Furthermore, we focus on the extensive crosstalk of caspases as a potential area of research on therapeutic strategies for treating EBI after SAH.

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“…Previous studies have found that in the early SAH stage, erythrocyte degradation products accumulated in the subarachnoid space, activating an inflammatory response and participating in the acceleration of brain injury (Schallner et al, 2015;Zhang et al, 2016). Both experimental studies and clinical trials have demonstrated that the aseptic inflammatory response after SAH can aggravate tissue damage and is an independent predictor of mortality in SAH patients (Pradilla et al, 2010;Muroi et al, 2011;Luo et al, 2021;Devlin et al, 2022). Microglia are innate immune cells of the central nervous system and can be activated rapidly under inflammatory conditions, trauma, or other stimulating factors.…”

Section: Melatonin and Inflammationmentioning

confidence: 99%

Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury

2022

Front. Aging Neurosci.

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Subarachnoid hemorrhage (SAH) is a common cerebrovascular disease with high mortality and disability rates. Despite progressive advances in drugs and surgical techniques, neurological dysfunction in surviving SAH patients have not improved significantly. Traditionally, vasospasm has been considered the main cause of death and disability following SAH, but anti-vasospasm therapy has not benefited clinical prognosis. Many studies have proposed that early brain injury (EBI) may be the primary factor influencing the prognosis of SAH. Melatonin is an indole hormone and is the main hormone secreted by the pineal gland, with low daytime secretion levels and high nighttime secretion levels. Melatonin produces a wide range of biological effects through the neuroimmune endocrine network, and participates in various physiological activities in the central nervous system, reproductive system, immune system, and digestive system. Numerous studies have reported that melatonin has extensive physiological and pharmacological effects such as anti-oxidative stress, anti-inflammation, maintaining circadian rhythm, and regulating cellular and humoral immunity. In recent years, more and more studies have been conducted to explore the molecular mechanism underlying melatonin-induced neuroprotection. The studies suggest beneficial effects in the recovery of intracerebral hemorrhage, cerebral ischemia-reperfusion injury, spinal cord injury, Alzheimer’s disease, Parkinson’s disease and meningitis through anti-inflammatory, antioxidant and anti-apoptotic mechanisms. This review summarizes the recent studies on the application and mechanism of melatonin in SAH.

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A Systematic Review of Inflammatory Cytokine Changes Following Aneurysmal Subarachnoid Hemorrhage in Animal Models and Humans

Cited by 12 publications

References 105 publications

NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

NLRP3 Inflammasome Overactivation in Patients with Aneurysmal Subarachnoid Hemorrhage

Biological Effects and Mechanisms of Caspases in Early Brain Injury after Subarachnoid Hemorrhage

Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury

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