Matrine treatment induced an A2 astrocyte phenotype and protected the blood-brain barrier in CNS autoimmunity

2021 ◽  
pp. 102004
Author(s):  
Yilei Jing ◽  
Rui Ma ◽  
Yaojuan Chu ◽  
Mengmeng Dou ◽  
Mengru Wang ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
Cns Autoimmunity

scholarly journals High-salt diet suppresses autoimmune demyelination by regulating the blood–brain barrier permeability

2021 ◽  
Vol 118 (12) ◽  
pp. e2025944118
Author(s):  
Shin-Young Na ◽  
Mathangi Janakiraman ◽  
Alexei Leliavski ◽  
Gurumoorthy Krishnamoorthy
Keyword(s):  
Autoimmune Disease ◽  
Blood Brain Barrier ◽  
High Salt ◽  
Brain Barrier ◽  
Chloride Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Blood Brain ◽  
Autoimmune Pathology ◽  
Cns Autoimmunity

Sodium chloride, “salt,” is an essential component of daily food and vitally contributes to the body’s homeostasis. However, excessive salt intake has often been held responsible for numerous health risks associated with the cardiovascular system and kidney. Recent reports linked a high-salt diet (HSD) to the exacerbation of artificially induced central nervous system (CNS) autoimmune pathology through changes in microbiota and enhanced TH17 cell differentiation [M. Kleinewietfeld et al., Nature 496, 518–522 (2013); C. Wu et al., Nature 496, 513–517 (2013); N. Wilck et al., Nature 551, 585–589 (2017)]. However, there is no evidence that dietary salt promotes or worsens a spontaneous autoimmune disease. Here we show that HSD suppresses autoimmune disease development in a mouse model of spontaneous CNS autoimmunity. We found that HSD consumption increased the circulating serum levels of the glucocorticoid hormone corticosterone. Corticosterone enhanced the expression of tight junction molecules on the brain endothelial cells and promoted the tightening of the blood–brain barrier (BBB) thereby controlling the entry of inflammatory T cells into the CNS. Our results demonstrate the multifaceted and potentially beneficial effects of moderately increased salt consumption in CNS autoimmunity.

B7-homologue 1 inhibits T cell-mediated blood–brain barrier disruption and regional encephalitogenicity in a spontaneous model of CNS autoimmunity

2014 ◽  
Vol 275 (1-2) ◽  
pp. 30
Author(s):  
Ivan Kuzmanov ◽  
Vilmos Posevitz ◽  
Stephanie Hucke ◽  
Daria Chudyka ◽  
Angela Dreykluft ◽  
...  
Keyword(s):  
T Cell ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Disruption ◽  
Blood Brain Barrier Disruption ◽  
Blood Brain ◽  
Cns Autoimmunity ◽  
Brain Barrier Disruption

scholarly journals Blood–brain barrier changes and cell invasion differ between therapeutic immune clearance of neurotrophic virus and CNS autoimmunity

2008 ◽  
Vol 105 (40) ◽  
pp. 15511-15516 ◽  
Author(s):  
Marzena J. Fabis ◽  
Timothy W. Phares ◽  
Rhonda B. Kean ◽  
Hilary Koprowski ◽  
D. Craig Hooper
Keyword(s):  
Blood Brain Barrier ◽  
Cell Invasion ◽  
Clinical Signs ◽  
Brain Barrier ◽  
Radical Scavenger ◽  
Neuroinflammatory Disease ◽  
Permeability Changes ◽  
Blood Brain ◽  
Cns Autoimmunity ◽  
Bbb Permeability

CNS tissues are protected from circulating cells and factors by the blood–brain barrier (BBB), a specialization of the neurovasculature. Outcomes of the loss of BBB integrity and cell infiltration into CNS tissues can differ vastly. For example, elevated BBB permeability is closely associated with the development of neurological disease in experimental allergic encephalomyelitis (EAE) but not during clearance of the attenuated rabies virus CVS-F3 from the CNS tissues. To probe whether differences in the nature of BBB permeability changes may contribute to the pathogenesis of acute neuroinflammatory disease, we compared the characteristics of BBB permeability changes in mice with EAE and in mice clearing CVS-F3. BBB permeability changes are largely restricted to the cerebellum and spinal cord in both models but differ in the extent of leakage of markers of different size and in the nature of cell accumulation in the CNS tissues. The accumulation in the CNS tissues of CD4 T cells expressing mRNAs specific for IFN-γ and IL-17 is common to both, but iNOS-positive cells invade into the CNS parenchyma only in EAE. Mice that have been immunized with myelin basic protein (MBP) and infected exhibit the features of EAE. Treatment with the peroxynitrite-dependent radical scavenger urate inhibits the invasion of iNOS-positive cells into the CNS tissues and the development of clinical signs of EAE without preventing the loss of BBB integrity in immunized/infected animals. These findings indicate that BBB permeability changes can occur in the absence of neuropathology provided that cell invasion is restricted.

Comparative in vivo and pathological analysis of the blood-brain barrier in mouse telencephalic transplants

1996 ◽  
Vol 22 (2) ◽  
pp. 118-128 ◽  
Author(s):  
S. Isenmann ◽  
S. Brandner ◽  
G. Kuhne ◽  
J. Boner ◽  
A. Aguzzi
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Pathological Analysis ◽  
Blood Brain

Conformationally Constrained Peptide Drugs Targeted at the Blood-Brain Barrier

1995 ◽  
Author(s):  
Thomas P. Davis ◽  
Thomas J. Abbruscato ◽  
Elizabeth Brownson ◽  
Victor J. Hruby
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Peptide Drugs ◽  
Conformationally Constrained ◽  
Blood Brain
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