scholarly journals CHANGES IN THE CONTENT OF IMMUNE CELLS CONTAINING THE FcR III RECEPTOR IN THE SLEEP AND BRAIN AFTER EXPERIMENTAL TBI

2020 ◽  
pp. 60-65
Author(s):  
Микола Лісяний ◽  
Настя Паламарьова ◽  
Людмила Бєльська ◽  
Антоніна Потапова
Keyword(s):  
Immune Cells ◽  
Craniocerebral Trauma ◽  
Brain Parenchyma ◽  
Immunomodulatory Activity ◽  
Left And Right ◽  
Immunomodulatory Drug ◽  
Immunomodulatory Properties ◽  
Low Levels ◽  
The Brain

At TBI there are disturbances in activity of immune system, can complicate regenerative and reparative responses in a brain. The aim of the study was to study the content of CD-16 cells in the spleen and brain parenchyma at different times after TBI in rats and in the correction of disorders in their composition by immunomodulatory drug galalite.Methods. Craniocerebral trauma in animals was modeled by dropping a load weighing 100 g from a height of 120 cm on the head of rats that were anesthetized and were in a state of narcotic sleep, which lasted up to 30 minutes. To correct the resulting disorders used immunomodulatory drug galavit at a dose of 2 mg / kg of animal weight in a volume of0.5 ml, which was administered intramuscularly to animals for 2, 3, 4 days after injury. The spleen and the left and right hemispheres of the brain were homogenized in 5.0 ml of medium 199 and suspensions containing 10.0x106 cells per 1 ml of medium 199 microglia were prepared and infiltrated CNS monocytes were prepared by the method of Sedgwick J. in co-authors. Determination of the level of CD-16 cells in suspensions of spleen and microglia was performed on a flow cytometer using monoclonal antibodies against CD-16 receptor company BD Biosciences according to the instructions for antibodies.Results. In mild TBI in rats, the number of CD- 16 cells containing the FcR III receptor decreases in the spleen for 2 to 5 days, and the number of these cells in the fractions of microglial cells increases. Galavit is a drug with immunomodulatory properties, has virtually no effect on low levels of CD-16 cells in the spleen and stimulates their accumulation in the brain for 10 days after TBI.Conclusions. The results indicate the effect of Galavit on the level of CD-16 cells in the spleen and brain, which indicates the immunomodulatory activity of this drug.

scholarly journals Microglial Function and Regulation during Development, Homeostasis and Alzheimer’s Disease

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 957
Author(s):  
Brad T. Casali ◽  
Erin G. Reed-Geaghan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immune Cells ◽  
Expression Patterns ◽  
Brain Parenchyma ◽  
Primary Role ◽  
And Function ◽  
Inflammatory Milieu ◽  
The Brain ◽  
Homeostatic State

Microglia are the resident immune cells of the brain, deriving from yolk sac progenitors that populate the brain parenchyma during development. During development and homeostasis, microglia play critical roles in synaptogenesis and synaptic plasticity, in addition to their primary role as immune sentinels. In aging and neurodegenerative diseases generally, and Alzheimer’s disease (AD) specifically, microglial function is altered in ways that significantly diverge from their homeostatic state, inducing a more detrimental inflammatory environment. In this review, we discuss the receptors, signaling, regulation and gene expression patterns of microglia that mediate their phenotype and function contributing to the inflammatory milieu of the AD brain, as well as strategies that target microglia to ameliorate the onset, progression and symptoms of AD.

Exploration of beneficial and deleterious effects of inflammation in stroke: dynamics of inflammation cells

2009 ◽  
Vol 367 (1908) ◽  
pp. 4699-4716 ◽  
Author(s):  
Taïssia Lelekov-Boissard ◽  
Guillemette Chapuisat ◽  
Jean-Pierre Boissel ◽  
Emmanuel Grenier ◽  
Marie-Aimée Dronne
Keyword(s):  
Immune Cells ◽  
Blood Cells ◽  
Inflammatory Process ◽  
Living Cells ◽  
Therapeutic Strategies ◽  
Brain Parenchyma ◽  
Brain Cell ◽  
Cytokines And Chemokines ◽  
The Brain

The inflammatory process during stroke consists of activation of resident brain microglia and recruitment of leucocytes, namely neutrophils and monocytes/macrophages. During inflammation, microglial cells, neutrophils and macrophages secrete inflammatory cytokines and chemokines, and phagocytize dead cells. The recruitment of blood cells (neutrophils and macrophages) is mediated by the leucocyte–endothelium interactions and more specifically by cell adhesion molecules. A mathematical model is proposed to represent the dynamics of various brain cells and of immune cells (neutrophils and macrophages). This model is based on a set of six ordinary differential equations and explores the beneficial and deleterious effects of inflammation, respectively phagocytosis by immune cells and the release of pro-inflammatory mediators and nitric oxide (NO). The results of our simulations are qualitatively consistent with those observed in experiments in vivo and would suggest that the increase of phagocytosis could contribute to the increase of the percentage of living cells. The inhibition of the production of cytokines and NO and the blocking of neutrophil and macrophage infiltration into the brain parenchyma led also to the improvement of brain cell survival. This approach may help to explore the respective contributions of the beneficial and deleterious roles of the inflammatory process in stroke, and to study various therapeutic strategies in order to reduce stroke damage.

scholarly journals Immune cells and CNS physiology: Microglia and beyond

2018 ◽  
Vol 216 (1) ◽  
pp. 60-70 ◽  
Author(s):  
Geoffrey T. Norris ◽  
Jonathan Kipnis
Keyword(s):  
Central Nervous System ◽  
Immune Cells ◽  
Brain Function ◽  
Brain Parenchyma ◽  
The Body ◽  
Immune Repertoire ◽  
Perivascular Macrophages ◽  
The Central Nervous System ◽  
Cns Immunity ◽  
The Brain

Recent advances have directed our knowledge of the immune system from a narrative of “self” versus “nonself” to one in which immune function is critical for homeostasis of organs throughout the body. This is also the case with respect to the central nervous system (CNS). CNS immunity exists in a segregated state, with a marked partition occurring between the brain parenchyma and meningeal spaces. While the brain parenchyma is patrolled by perivascular macrophages and microglia, the meningeal spaces are supplied with a diverse immune repertoire. In this review, we posit that such partition allows for neuro–immune crosstalk to be properly tuned. Convention may imply that meningeal immunity is an ominous threat to brain function; however, recent studies have shown that its presence may instead be a steady hand directing the CNS to optimal performance.

scholarly journals Aquaporin-4 Expression during Toxic and Autoimmune Demyelination

Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2187
Author(s):  
Sven Olaf Rohr ◽  
Theresa Greiner ◽  
Sarah Joost ◽  
Sandra Amor ◽  
Paul van der Valk ◽  
...  
Keyword(s):  
Immune Cells ◽  
Water Channel ◽  
Staining Intensity ◽  
Brain Parenchyma ◽  
Aquaporin 4 ◽  
Aqp4 Expression ◽  
Humoral Immune ◽  
Autoimmune Demyelination ◽  
Peripheral Immune Cells ◽  
The Brain

The water channel protein aquaporin-4 (AQP4) is required for a normal rate of water exchange across the blood–brain interface. Following the discovery that AQP4 is a possible autoantigen in neuromyelitis optica, the function of AQP4 in health and disease has become a research focus. While several studies have addressed the expression and function of AQP4 during inflammatory demyelination, relatively little is known about its expression during non-autoimmune-mediated myelin damage. In this study, we used the toxin-induced demyelination model cuprizone as well as a combination of metabolic and autoimmune myelin injury (i.e., Cup/EAE) to investigate AQP4 pathology. We show that during toxin-induced demyelination, diffuse AQP4 expression increases, while polarized AQP4 expression at the astrocyte endfeet decreases. The diffuse increased expression of AQP4 was verified in chronic-active multiple sclerosis lesions. Around inflammatory brain lesions, AQP4 expression dramatically decreased, especially at sites where peripheral immune cells penetrate the brain parenchyma. Humoral immune responses appear not to be involved in this process since no anti-AQP4 antibodies were detected in the serum of the experimental mice. We provide strong evidence that the diffuse increase in anti-AQP4 staining intensity is due to a metabolic injury to the brain, whereas the focal, perivascular loss of anti-AQP4 immunoreactivity is mediated by peripheral immune cells.

scholarly journals Microglia-specific overexpression of α-synuclein leads to severe dopaminergic neurodegeneration by phagocytic exhaustion and oxidative toxicity

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Simone Bido ◽  
Sharon Muggeo ◽  
Luca Massimino ◽  
Matteo Jacopo Marzi ◽  
Serena Gea Giannelli ◽  
...  
Keyword(s):  
Immune Cells ◽  
Neuronal Degeneration ◽  
Brain Parenchyma ◽  
Microglial Cells ◽  
Dopaminergic Neurodegeneration ◽  
Progressive Degeneration ◽  
Toxic Environment ◽  
Inflammatory State ◽  
Peripheral Immune Cells ◽  
The Brain

AbstractRecent findings in human samples and animal models support the involvement of inflammation in the development of Parkinson’s disease. Nevertheless, it is currently unknown whether microglial activation constitutes a primary event in neurodegeneration. We generated a new mouse model by lentiviral-mediated selective α-synuclein (αSYN) accumulation in microglial cells. Surprisingly, these mice developed progressive degeneration of dopaminergic (DA) neurons without endogenous αSYN aggregation. Transcriptomics and functional assessment revealed that αSYN-accumulating microglial cells developed a strong reactive state with phagocytic exhaustion and excessive production of oxidative and proinflammatory molecules. This inflammatory state created a molecular feed-forward vicious cycle between microglia and IFNγ-secreting immune cells infiltrating the brain parenchyma. Pharmacological inhibition of oxidative and nitrosative molecule production was sufficient to attenuate neurodegeneration. These results suggest that αSYN accumulation in microglia induces selective DA neuronal degeneration by promoting phagocytic exhaustion, an excessively toxic environment and the selective recruitment of peripheral immune cells.

scholarly journals Noradrenergic signaling in wakeful states inhibits microglial surveillance and synaptic plasticity in the mouse visual cortex

2019 ◽  
Author(s):  
Rianne D. Stowell ◽  
Grayson O. Sipe ◽  
Ryan P. Dawes ◽  
Hanna N. Batchelor ◽  
Katheryn A. Lordy ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Immune Cells ◽  
Neural Activity ◽  
Adrenergic Receptors ◽  
Brain Parenchyma ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Mouse Visual Cortex ◽  
The Brain

AbstractMicroglia are the innate immune cells of the brain with roles in neuroimmunology and synaptic plasticity. Microglial processes continuously survey the brain parenchyma interacting with synaptic elements and maintaining tissue homeostasis. However, the mechanisms that control surveillance and its role in synaptic plasticity are poorly understood. Microglial dynamics in vivo have been primarily studied in anesthetized animals, where slow-wave neural activity resembles sleep-like states. We report that microglial surveillance and injury response in awake animals are reduced compared to when animals are anesthetized, suggesting that arousal state profoundly modulates microglial roles in the physiological brain. Stimulating β2-adrenergic receptors recapitulated these observations and also disrupted experience-dependent plasticity only when intact β2-adrenergic receptors were present in microglia specifically. These results indicate that microglial roles in surveillance and synaptic plasticity in the healthy brain are modulated by noradrenergic fluctuations between arousal states and raises new considerations for sleep/wake disruption in neurodevelopment and neuropathology.

Advantages of Complementary Stereo Images as Viewed with the Low-Temperature Field-Emission SEM

1992 ◽  
Vol 50 (2) ◽  
pp. 1314-1315
Author(s):  
William P. Wergin ◽  
Eric F. Erbe
Keyword(s):  
Fold Increase ◽  
Horizontal Displacement ◽  
Three Dimensions ◽  
Stereo Image ◽  
Stereo Pair ◽  
Sem Micrograph ◽  
Left And Right ◽  
The Common ◽  
The Brain ◽  
Pair Analysis

The eye-brain complex allows those of us with normal vision to perceive and evaluate our surroundings in three-dimensions (3-D). The principle factor that makes this possible is parallax - the horizontal displacement of objects that results from the independent views that the left and right eyes detect and simultaneously transmit to the brain for superimposition. The common SEM micrograph is a 2-D representation of a 3-D specimen. Depriving the brain of the 3-D view can lead to erroneous conclusions about the relative sizes, positions and convergence of structures within a specimen. In addition, Walter has suggested that the stereo image contains information equivalent to a two-fold increase in magnification over that found in a 2-D image. Because of these factors, stereo pair analysis should be routinely employed when studying specimens.Imaging complementary faces of a fractured specimen is a second method by which the topography of a specimen can be more accurately evaluated.

ADRENOCORTICAL FUNCTION IN PATIENTS WITH ACUTE SEVERE BRAIN AND PITUITARY LESION

1962 ◽  
Vol 40 (2) ◽  
pp. 254-262 ◽  
Author(s):  
H. H. Bassøe ◽  
R. Emberland ◽  
E. Glück ◽  
K. F. Støa
Keyword(s):  
Pituitary Gland ◽  
Adrenal Cortex ◽  
Artificial Ventilation ◽  
Practical Significance ◽  
Adrenocortical Function ◽  
The Third ◽  
Low Levels ◽  
Pituitary Lesion ◽  
Steroid Excretion ◽  
The Brain

ABSTRACT The steroid excretion and the plasma corticosteroids were investigated in three patients with necrosis of the brain and of the pituitary gland. The patients were kept alive by artificial ventilation. In two of the patients the neutral 17-ketosteroids and the 17-hydrocorticosteroids fell to extremely low levels. At the same time, the number of eosinophil cells showed a tendency to increase. Corticotrophin administered intravenously twice to the third patient had a stimulating effect on the adrenal cortex. The theoretical and practical significance of these findings is discussed.

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