Expression of mRNAs for IL-1β, IL-6, IL-10, TNFα, CX3CL1, and TGFβ1 Cytokines in the Brain Tissues: Assessment of Contribution of Blood Cells with and without Perfusion

Kvichansky, A. A.; Volobueva, Maria N; Spivak, Yu. S.; Tret’yakova, L. V.; Gulyaeva, N. V.; Bolshakov, A D

doi:10.1134/s0006297919080066

Cited by 12 publications

(4 citation statements)

References 15 publications

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“…Those that are produced by peripheral immune cells and cross the blood-brain-barrier, and those that are produced by CNS resident cells, namely the neurons and glial cells. [13][14][15][16] Cytokines produced by neurons and glial cells within the brain may participate in the complex autonomic, neuroendocrine, metabolic, and behavioral responses to infection, inflammation, ischemia, and other brain injuries. [16][17][18] The physiological importance of proinflammatory cytokines such as interferon-γ (IFN-γ) lies in its function in regulating immune and inflammatory events.…”

Section: Introductionmentioning

confidence: 99%

Interferon-Gamma and Interleukin-1Beta Enhance the Secretion of Brain-Derived Neurotrophic Factor and Promotes the Survival of Cortical Neurons in Brain Injury

2020

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Neuro-inflammation is associated with the production of cytokines, which influence neuronal and glial functions. Although the proinflammatory cytokines interferon-γ (IFN-γ) and interleukin-1Beta (IL-1β) are thought to be the major mediators of neuro-inflammation, their role in brain injury remains ill-defined. The objective of this study was to examine the effect of IFN-γ and IL-1β on survival of cortical neurons in stab wound injury in mice. A stab wound injury was made in the cortex of male BALB/c mice. Injured mice (I) were divide into IFN-γ and IL-1β treatment experiments. Mice in I + IFN-γ group were treated with IFN-γ (ip, 10 µg/kg/day) for 1, 3 and 7 days and mice in I + IL-1β group were treated with 5 IP injection of IL-1β (0.5 µg /12 h). Appropriate control mice were maintained for comparison. Immunostaining of frozen brain sections for astrocytes (GFAP), microglia (Iba-1) and Fluoro-Jade B staining for degenerating neurons were used. Western blotting and ELISA for brain-derived neurotrophic factor (BDNF) were done on the tissues isolated from the injured sites. Results showed a significant increase in the number of both astrocytes and microglia in I + IFN-γ and I + IL-1β groups. There were no significant changes in the number of astrocytes or microglia in noninjury groups (NI) treated with IFN-γ or IL-1β. The number of degenerating neurons significantly decreased in I + IFN-γ and I + IL-1β groups. GFAP and BDNF levels were significantly increased in I + IFN-γ and I + IL-1β groups. Interferon-γ and IL-1β induce astrogliosis, microgliosis, enhance the secretion of BDNF, one of the many neurotrophic factors after brain injury, and promote the survival of cortical neurons in stab wound brain injury.

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Section: Introductionmentioning

confidence: 99%

Interferon-Gamma and Interleukin-1Beta Enhance the Secretion of Brain-Derived Neurotrophic Factor and Promotes the Survival of Cortical Neurons in Brain Injury

2020

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“…[94] Claudin-5 is an integral membrane protein and an essential component of the tight junction protein complex that constitutes the BBB. [95] Anke et al also showed that claudin-5 methylation was associated with cognitive impairment. [96] IL-1β and TNF-α are strongly involved in BBB disruption through epigenetics.…”

Section: Resultsmentioning

confidence: 99%

Postoperative delirium, neuroinflammation, and influencing factors of postoperative delirium: A review

et al. 2023

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Postoperative delirium (POD) is an acute cognitive dysfunction that is mainly characterized by memory impairment and disturbances in consciousness. POD can prolong the hospital stay and increase the 1-month mortality rate of patients. The overall incidence of POD is approximately 23%, and its prevalence can go up to 50% in high-risk surgeries. Neuroinflammation is an important pathogenic mechanism of POD that mediates microglial activation and leads to synaptic remodeling. Neuroinflammation, as an indispensable pathogenesis of POD, can occur due to a variety of factors, including aseptic inflammation caused by surgery, effects of anesthetic drugs, disruption of the blood-brain barrier, and epigenetics. Understanding these factors and avoiding the occurrence of risk factors may help prevent POD in time. This review provides a brief overview of POD and neuroinflammation and summarizes various factors affecting POD development mediated by neuroinflammation, which may serve as future targets for the prevention and treatment of POD.

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“…The meninges are known to contain resident immune cells [ 30 ] and a single CSD rapidly activates meningeal macrophages [ 19 ]. Leptomeningeal mRNA levels of immune markers are not affected by non-resident cells although in the cortical parenchyma and dura mater blood cells contribute to the total mRNA pool of inflammatory mediators [ 31 ]. Activated pial macrophages can release pro- and anti-inflammatory factors into the subarachnoid space contributing to induction and resolution of inflammation, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…Cortical neurons release fractalkine that acts on its cognate microglial receptors CX3CR1. Resident meningeal macrophages also express fractalkine receptor CX3CR1 [ 21 , 30 ] and leptomeninges exhibit constitutive expression of CX3CL1 [ 31 ]. Given that fractalkine inhibits microglial activation and suppresses production of proinflammatory cytokines in the healthy CNS [ 40 ], meningeal downregulation of Cx3cl1 may contribute to chronic meningeal inflammation triggered by cannula implantation.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory response of leptomeninges to a single cortical spreading depolarization

Karan,

Gerasimov,

Spivak

et al. 2024

J Headache Pain

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Background Neurogenic meningeal inflammation is regarded as a key driver of migraine headache. Multiple evidence show importance of inflammatory processes in the dura mater for pain generation but contribution of the leptomeninges is less clear. We assessed effects of cortical spreading depolarization (CSD), the pathophysiological mechanism of migraine aura, on expression of inflammatory mediators in the leptomeninges. Methods A single CSD event was produced by a focal unilateral microdamage of the cortex in freely behaving rats. Three hours later intact cortical leptomeninges and parenchyma of ipsi-lesional (invaded by CSD) and sham-treated contra-lesional (unaffected by CSD) hemispheres were collected and mRNA levels of genes associated with inflammation (Il1b, Tnf, Ccl2; Cx3cl1, Zc3h12a) and endocannabinoid CB2 receptors (Cnr2) were measured using qPCR. Results Three hours after a single unilateral CSD, most inflammatory factors changed their expression levels in the leptomeninges, mainly on the side of CSD. The meninges overlying affected cortex increased mRNA expression of all proinflammatory cytokines (Il1b, Tnf, Ccl2) and anti-inflammatory factors Zc3h12a and Cx3cl1. Upregulation of proinflammatory cytokines was found in both meninges and parenchyma while anti-inflammatory markers increased only meningeal expression. Conclusion A single CSD is sufficient to produce pronounced leptomeningeal inflammation that lasts for at least three hours and involves mostly meninges overlying the cortex affected by CSD. The prolonged post-CSD inflammation of the leptomeninges can contribute to mechanisms of headache generation following aura phase of migraine attack.

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Expression of mRNAs for IL-1β, IL-6, IL-10, TNFα, CX3CL1, and TGFβ1 Cytokines in the Brain Tissues: Assessment of Contribution of Blood Cells with and without Perfusion

Cited by 12 publications

References 15 publications

Interferon-Gamma and Interleukin-1Beta Enhance the Secretion of Brain-Derived Neurotrophic Factor and Promotes the Survival of Cortical Neurons in Brain Injury

Interferon-Gamma and Interleukin-1Beta Enhance the Secretion of Brain-Derived Neurotrophic Factor and Promotes the Survival of Cortical Neurons in Brain Injury

Postoperative delirium, neuroinflammation, and influencing factors of postoperative delirium: A review

Inflammatory response of leptomeninges to a single cortical spreading depolarization

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