scholarly journals The anatomy and immunology of vasculature in the central nervous system

2019 ◽  
Vol 4 (37) ◽  
pp. eaav0492 ◽  
Author(s):  
Panagiotis Mastorakos ◽  
Dorian McGavern
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Steady State ◽  
Cerebral Ischemia ◽  
Autoimmune Disease ◽  
Immune Responses ◽  
Anatomical Variations ◽  
Structural Variations ◽  
Cerebrovascular Injury ◽  
The Central Nervous System

Barriers between circulation and the central nervous system (CNS) play a key role in the development and modulation of CNS immune responses. Structural variations in the vasculature traversing different anatomical regions within the CNS strongly influence where and how CNS immune responses first develop. Here, we provide an overview of cerebrovascular anatomy, focusing on the blood-CNS interface and how anatomical variations influence steady-state immunology in the compartment. We then discuss how CNS vasculature is affected by and influences the development of different pathophysiological states, such as CNS autoimmune disease, cerebrovascular injury, cerebral ischemia, and infection.

Effects of hypercapnia and hypoxia on inspiratory and expiratory diaphragmatic activity in conscious cats

1994 ◽  
Vol 77 (4) ◽  
pp. 1644-1652 ◽  
Author(s):  
M. Bonora ◽  
M. Boule
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Steady State ◽  
Electromyographic Activity ◽  
Large Reduction ◽  
Before And After ◽  
The Central Nervous System ◽  
State Changes ◽  
Chemical Stimuli ◽  
Adult Cats

The influence of steady-state changes in chemical stimuli on ventilation and electromyographic activity of the diaphragm during both inspiration (total DI) and expiration (total DE) was studied in unanesthetized intact adult cats before and after carotid denervation. In intact animals, during hypercapnia (2 4, and 6% CO2), tidal volume (VT) and total DI increase, whereas total DE did not consistently change. During ambient hypocapnic hypoxia (14, 12, and 10% O2), VT increased only at 10% O2, whereas total DI increased at all levels studied. Total DE increased substantially at 14% O2, persisting up to the end of expiration with 12 and 10% O2. This effect was markedly attenuated during normocapnic hypoxia. During CO hypoxemia (1,700 ppm in air), VT as well as total DI and total DE decreased because of a large reduction in inspiratory and expiratory time elicited by tachypneic breathing. The effects of hypercapnia and hypoxia persisted after carotid denervation. Therefore, 1) in contrast to hypercapnia, hypoxia markedly enhances the expiratory diaphragmatic activity, 1) this expiratory braking mechanism depends on the severity of hypoxia and is partly due to hypocapnia secondary to hypoxia; and 3) because this effect was observed after carotid denervation and during CO hypoxemia, it may arise in the central nervous system, possibly in bulbopontine structures.

The Immunobiology of Multiple Sclerosis: An Autoimmune Disease of the Central Nervous System

1999 ◽  
Vol 6 (3) ◽  
pp. 149-166 ◽  
Author(s):  
Paul Conlon ◽  
Jorge R. Oksenberg ◽  
Jingwu Zhang ◽  
Lawrence Steinman
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Autoimmune Disease ◽  
The Central Nervous System

The role of macrophage subpopulations in autoimmune disease of the central nervous system

1996 ◽  
Vol 28 (2) ◽  
pp. 83-97 ◽  
Author(s):  
Jan Bauer ◽  
Sigrid R. Ruuls ◽  
Ingeborg Huitinga ◽  
Christine D. Dijkstra
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Autoimmune Disease ◽  
Macrophage Subpopulations ◽  
The Central Nervous System

scholarly journals Protective immune responses against West Nile virus are primed by distinct complement activation pathways

2006 ◽  
Vol 203 (5) ◽  
pp. 1371-1381 ◽  
Author(s):  
Erin Mehlhop ◽  
Michael S. Diamond
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
West Nile Virus ◽  
Immune Responses ◽  
Complement Activation ◽  
Adaptive Immune Responses ◽  
Cell Responses ◽  
Adaptive Immune ◽  
The Central Nervous System ◽  
Activation Pathways

West Nile virus (WNV) causes a severe infection of the central nervous system in several vertebrate animals including humans. Prior studies have shown that complement plays a critical role in controlling WNV infection in complement (C) 3−/− and complement receptor 1/2−/− mice. Here, we dissect the contributions of the individual complement activation pathways to the protection from WNV disease. Genetic deficiencies in C1q, C4, factor B, or factor D all resulted in increased mortality in mice, suggesting that all activation pathways function together to limit WNV spread. In the absence of alternative pathway complement activation, WNV disseminated into the central nervous system at earlier times and was associated with reduced CD8+ T cell responses yet near normal anti-WNV antibody profiles. Animals lacking the classical and lectin pathways had deficits in both B and T cell responses to WNV. Finally, and somewhat surprisingly, C1q was required for productive infection in the spleen but not for development of adaptive immune responses after WNV infection. Our results suggest that individual pathways of complement activation control WNV infection by priming adaptive immune responses through distinct mechanisms.

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