Autoimmunity in acute ischemic stroke and the role of blood-brain barrier: the dark side or the light one?

Tsygan, N. V.; Trashkov, Alexander P.; Litvinenko, Igor; Yakovleva, V. A.; Ryabtsev, Aleksander V.; Vasiliev, Andrei G.; Чурилов, Леонид Павлович

doi:10.1007/s11684-019-0688-6

Cited by 26 publications

(20 citation statements)

References 46 publications

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“…In aSAH rodent model studies, glymphatic channel disruption was found to promote perivascular neuroinflammation due to accumulation of heme waste products in the subarachnoid space [ 42 , 43 ]. Disruption of the blood–brain barrier and glymphatic system in stroke may facilitate the exposure of brain-specific antigens to the adaptive immune system, in turn inducing autoimmune disorders, resulting in chronic inflammation and, potentially, dementia [ 44 ].…”

Section: Neuroimmune Axes In Asahmentioning

confidence: 99%

Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage

Chai

Kuo

2023

IJMS

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Aneurysmal subarachnoid hemorrhage (aSAH) is one of the most severe neurological disorders, with a high mortality rate and severe disabling functional sequelae. Systemic inflammation following hemorrhagic stroke may play an important role in mediating intracranial and extracranial tissue damage. Previous studies showed that various systemic inflammatory biomarkers might be useful in predicting clinical outcomes. Anti-inflammatory treatment might be a promising therapeutic approach for improving the prognosis of patients with aSAH. This review summarizes the complicated interactions between the nervous system and the immune system.

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Section: Neuroimmune Axes In Asahmentioning

confidence: 99%

Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage

Chai

Kuo

2023

IJMS

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“…It is unknown if the pathological reaction originates in or is driven from the inside or outside of the protected nervous system. The latter is an important point as the traditionally considered protective space of the nervous system may have a role in forming the autoimmune GBS pathology due to an inability to formulate an effective, self-extinguishing resolution of the immune system activation [51,52]. The intersection between COVID-19 and GBS may provide insight as to how the nervous system responds to viral illness and critical care illnesses.…”

Section: Inflammationmentioning

confidence: 99%

Guillain–Barré Syndrome in COVID-19—The Potential Role of NCAM-1 and Immunotherapy

Laudański

Yakhkind

Restrepo

et al. 2021

BioMed

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Coronavirus disease 2019 (COVID-19) interacts with the nervous system directly and indirectly by affecting the activation of the immune system. Guillain–Barré syndrome (GBS) is triggered by an inappropriate immune system activation that overlaps with the neurotoxic mechanism of an invading pathogen. Here, we discuss the complexity of an abnormal immune system response leading to the generation of autoimmunity in the setting of acute viral infection. A 67-year-old male patient with COVID-19 developed a sensory motor acute polyneuropathy with respiratory failure. Several serum inflammatory and neurodegeneration markers were collected during hospital days 1, 3, 8, and 67 and compared to healthy individuals. Neural cell adhesion molecule 1 (NCAM-1) and neurofilament light chain (NfL) values were highly variable when compared to healthy individuals, but not to the reference COVID-19 group. We focused our attention on NCAM-1 as a possible target for antibodies directed at COVID-19 in silico.

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“…In the AIS there is an imbalance of the cytokines with a deficiency of anti-inflammatory cytokines and an increase in the triad of pro-inflammatory cytokines such as Tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and IL-6, which are produced by both microglial cells and immunocompetent peripheral blood cells, as evidenced by an increase in the concentration of these cytokines in the serum of patients with AIS (13). TNF-α is a pleiotropic cytokine that plays a key role in many physiological and pathological cellular processes, apoptosis and autophagy are complex multi-level processes, in the regulation of contents in the peripheral blood (2,10,12,14). Thus, the signal for the activation of apoptosis and autophagy in peripheral blood cells can be received from several mediators of the immune response and neuroinflammation, the increased production of which in response to ischemic injury occurs not only in the lesion but also in the peripheral blood.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the signal for the activation of apoptosis and autophagy in peripheral blood cells can be received from several mediators of the immune response and neuroinflammation, the increased production of which in response to ischemic injury occurs not only in the lesion but also in the peripheral blood. Mediators that induce the activation of apoptosis in peripheral blood are TNF-α, IL-1β, soluble Fas ligand, and heat shock proteins-70 (14). Autophagy is involved in the regulation of the production of pro-inflammatory cytokines (IL-1β, IL-17, IL-18, IL-23, and chemokine (C-X-C motif) ligand 1 (10).…”

Section: Discussionmentioning

confidence: 99%

Expression of autophagy and apoptosis biomarkers in patients with acute ischemic stroke

Mamytov¹,

Mamytova²,

Toktomametova³

et al. 2022

Biomedicine

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Introduction and Aim: Apoptosis, autophagy, and necrosis are the main mechanisms of neuron death in acute ischemic stroke (AIS). This study aimed to evaluate the expression of apoptosis and autophagy biomarkers in peripheral blood of patients with AIS. Materials and Methods: Sixty-eight patients (32 men and 36 women) aged 30-60 years with AIS underwent a clinical and neurological examination on the 1st, 7th, and 14th days after the disease onset. The expression of apoptosis and autophagy biomarkers in peripheral blood was evaluated by flow cytometry and compared with the severity of neurological deficit and injury on the 1st, 7th, and 14th days, using correlation analysis. Results: There is a statistical significance compared with the control group and an increase in the expression of key biomarkers of apoptosis and autophagy was revealed. Increased expression levels of annexin A5 and caspase-3 positively correlate with the severity of neurological deficit and injury on the 1st and 7th days from the onset of the disease. Conclusion: A direct correlation was revealed between elevated levels of apoptosis and autophagy biomarkers in peripheral blood and severity of neurological deficit and injury on the 1st, 7th, and 14th days from the onset of AIS.

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Autoimmunity in acute ischemic stroke and the role of blood-brain barrier: the dark side or the light one?

Cited by 26 publications

References 46 publications

Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage

Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage

Guillain–Barré Syndrome in COVID-19—The Potential Role of NCAM-1 and Immunotherapy

Expression of autophagy and apoptosis biomarkers in patients with acute ischemic stroke

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