scholarly journals Acid-Sensing Ion Channels: Expression and Function in Resident and Infiltrating Immune Cells in the Central Nervous System

2021 ◽  
Vol 15 ◽  
Author(s):  
Victoria S. Foster ◽  
Lachlan D. Rash ◽  
Glenn F. King ◽  
Michelle M. Rank
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ion Channels ◽  
Immune Cells ◽  
Cell Function ◽  
Immune Cell ◽  
Immune Cell Function ◽  
Acid Sensing Ion Channels ◽  
The Central Nervous System ◽  
Tissue Acidosis

Peripheral and central immune cells are critical for fighting disease, but they can also play a pivotal role in the onset and/or progression of a variety of neurological conditions that affect the central nervous system (CNS). Tissue acidosis is often present in CNS pathologies such as multiple sclerosis, epileptic seizures, and depression, and local pH is also reduced during periods of ischemia following stroke, traumatic brain injury, and spinal cord injury. These pathological increases in extracellular acidity can activate a class of proton-gated channels known as acid-sensing ion channels (ASICs). ASICs have been primarily studied due to their ubiquitous expression throughout the nervous system, but it is less well recognized that they are also found in various types of immune cells. In this review, we explore what is currently known about the expression of ASICs in both peripheral and CNS-resident immune cells, and how channel activation during pathological tissue acidosis may lead to altered immune cell function that in turn modulates inflammatory pathology in the CNS. We identify gaps in the literature where ASICs and immune cell function has not been characterized, such as neurotrauma. Knowledge of the contribution of ASICs to immune cell function in neuropathology will be critical for determining whether the therapeutic benefits of ASIC inhibition might be due in part to an effect on immune cells.

scholarly journals Developmental maturation of innate immune cell function correlates with susceptibility to central nervous system autoimmunity

2013 ◽  
Vol 43 (8) ◽  
pp. 2078-2088 ◽  
Author(s):  
Deetje Hertzenberg ◽  
Klaus Lehmann-Horn ◽  
Silke Kinzel ◽  
Veronika Husterer ◽  
Petra D. Cravens ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Function ◽  
Immune Cell ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Immune Cell Function ◽  
Developmental Maturation

scholarly journals Cell Volume Regulation in Immune Cell Function, Activation and Survival

2021 ◽  
Vol 55 (S1) ◽  
pp. 71-88
Keyword(s):  
Ion Channels ◽  
Ion Transport ◽  
Cell Volume ◽  
Immune Cells ◽  
Volume Regulation ◽  
Cell Function ◽  
Immune Cell ◽  
Regulatory Mechanisms ◽  
Immune Cell Function ◽  
Volume Decrease

The regulation of cell volume is an essential cellular process in nearly every living organism. The importance of volume regulation in immune cells cannot be understated, as it ensures proper cellular function and effective immune response. These cells utilize ion channels and transporters to maintain volume homeostasis through rapid ion transport across the cell membrane. Immune cells express mechanisms controlling regulatory volume decrease (RVD), regulatory volume increase (RVI), proliferative RVD, and apoptotic volume decrease (AVD). In this review, we summarize recent studies examining the importance of several ion channels, particularly potassium and chloride channels in regulating ion transport during osmotic stress, and in immune cell function, activation, proliferation, and death. We also review the key mechanisms functioning in immune cell proliferation and apoptosis. They serve a crucial role in maintaining adequate ionic concentrations, mediating immune cell activation, and generating proliferative pathways. These regulatory mechanisms play key roles in the function and survival of immune cells, as impaired volume regulation contributes to the pathophysiology of various disorders. A complete understanding of immune cell volume regulatory mechanisms may be a starting point for the development of therapeutic agents targeting these ion channels to treat inflammatory diseases.

scholarly journals Increased Levels of IL-16 in the Central Nervous System during Neuroinflammation Are Associated with Infiltrating Immune Cells and Resident Glial Cells

Biology ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 472
Author(s):  
Shehla U Hridi ◽  
Mark Barbour ◽  
Chelsey Wilson ◽  
Aimee JPM Franssen ◽  
Tanith Harte ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Cells ◽  
Immune Cell ◽  
Demyelinating Disease ◽  
Autoimmune Encephalomyelitis ◽  
Cellular Source ◽  
The Central Nervous System ◽  
Phosphate Buffered Saline ◽  
Brain And Spinal Cord

Interleukin (IL)-16, a CD4+ immune cell specific chemoattractant cytokine, has been shown to be involved in the development of multiple sclerosis, an inflammatory demyelinating disease of the central nervous system (CNS). While immune cells such as T cells and macrophages are reported to be the producers of IL-16, the cellular source of IL-16 in the CNS is less clear. This study investigates the correlation of IL-16 expression levels in the CNS with the severity of neuroinflammation and determines the phenotype of cells which produce IL-16 in the CNS of experimental autoimmune encephalomyelitis (EAE) mice. Our data show that IL-16 expression is significantly increased in the brain and spinal cord tissues of EAE mice compared to phosphate buffered saline (PBS) immunised controls. Dual immunofluorescence staining reveals that the significantly increased IL-16+ cells in the CNS lesions of EAE mice are likely to be the CD45+ infiltrating immune cells such as CD4+ or F4/80+ cells and the CNS resident CD11b+ microglia and GFAP+ astrocytes, but not NeuN+ neurons. Our data suggest cytokine IL-16 is closely involved in EAE pathology as evidenced by its increased expression in the glial and infiltrating immune cells, which impacts the recruitment and activation of CD4+ immune cells in the neuroinflammation.

scholarly journals Neurological and mental health consequences of COVID-19: potential implications for well-being and labor force

2021 ◽  
Author(s):  
I B Meier ◽  
C Vieira Ligo Teixeira ◽  
I Tarnanas ◽  
F Mirza ◽  
L Rajendran
Keyword(s):  
Mental Health ◽  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Impairment ◽  
Immune Cell ◽  
Previous History ◽  
Well Being ◽  
Acute Disseminated Encephalomyelitis ◽  
The Central Nervous System ◽  
Neurological Protection

Abstract Recent case studies show that the SARS-CoV-2 infectious disease, COVID-19, is associated with accelerated decline of mental health, in particular, cognition in elderly individuals, but also with neurological and neuropsychiatric illness in young people. Recent studies also show a bidirectional link between COVID-19 and mental health in that people with previous history of psychiatric illness have a higher risk for contracting COVID-19 and that COVID-19 patients display a variety of psychiatric illnesses. Risk factors and the response of the central nervous system to the virus show large overlaps with pathophysiological processes associated with Alzheimer’s disease, delirium, post-operative cognitive dysfunction and acute disseminated encephalomyelitis, all characterized by cognitive impairment. These similarities lead to the hypothesis that the neurological symptoms could arise from neuroinflammation and immune cell dysfunction both in the periphery as well as in the central nervous system and the assumption that long-term consequences of COVID-19 may lead to cognitive impairment in the well-being of the patient and thus in today’s workforce, resulting in large loss of productivity. Therefore, particular attention should be paid to neurological protection during treatment and recovery of COVID-19, while cognitive consequences may require monitoring.

Inflammatory Mechanisms in Parkinson’s Disease: From Pathogenesis to Targeted Therapies

2021 ◽  
pp. 107385842199226
Author(s):  
Stellina Y. H. Lee ◽  
Nathanael J. Yates ◽  
Susannah J. Tye
Keyword(s):  
Parkinson’S Disease ◽  
Central Nervous System ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Immune Cells ◽  
Critical Factor ◽  
Neurodegenerative Process ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
Novel Target

Inflammation is a critical factor contributing to the progressive neurodegenerative process observed in Parkinson’s disease (PD). Microglia, the immune cells of the central nervous system, are activated early in PD pathogenesis and can both trigger and propagate early disease processes via innate and adaptive immune mechanisms such as upregulated immune cells and antibody-mediated inflammation. Downstream cytokines and gene regulators such as microRNA (miRNA) coordinate later disease course and mediate disease progression. Biomarkers signifying the inflammatory and neurodegenerative processes at play within the central nervous system are of increasing interest to clinical teams. To be effective, such biomarkers must achieve the highest sensitivity and specificity for predicting PD risk, confirming diagnosis, or monitoring disease severity. The aim of this review was to summarize the current preclinical and clinical evidence that suggests that inflammatory processes contribute to the initiation and progression of neurodegenerative processes in PD. In this article, we further summarize the data about main inflammatory biomarkers described in PD to date and their potential for regulation as a novel target for disease-modifying pharmacological strategies.

scholarly journals Complement facilitates developmental microglial pruning of astrocyte and vascular networks

2022 ◽  
Author(s):  
Gopalan Gnanaguru ◽  
Steven J Tabor ◽  
Kentaro Yuda ◽  
Ryo Mukai ◽  
Jörg Köhl ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Cell ◽  
Vascular Density ◽  
Vascular Networks ◽  
Vascular Patterning ◽  
Vascular Growth ◽  
Vascular Bed ◽  
Retinal Microglia ◽  
The Central Nervous System

Microglia, the resident immune cell of the central nervous system, play a pivotal role in facilitating neurovascular development through mechanisms that are not fully understood. This current work resolves a previously unknown role for microglia in facilitating the developmental pruning of the astrocytic template resulting in a spatially organized retinal vascular bed. Mechanistically, our study identified that local microglial expression of complement (C)3 and C3aR is necessary for the regulation of astrocyte patterning and vascular growth during retinal development. Ablation of retinal microglia, loss of C3 or C3aR reduced developmental pruning and clearance of astrocytic bodies leading to increased astrocyte density leading to altered vascular patterning during retinal vascular development. This data demonstrates that C3/C3aR signaling is an important checkpoint required for the finetuning of vascular density during neuroretinal development.

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