Primary carcinoma of the choroid plexus with metastatic dissemination within the central nervous system

1979 ◽  
Vol 51 (1-2) ◽  
pp. 105-111 ◽  
Author(s):  
J. Vaquero ◽  
J. Cabezudo ◽  
G. Leunda ◽  
R. Carrillo ◽  
J. Garc�a Ur�a
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Choroid Plexus ◽  
Primary Carcinoma ◽  
Metastatic Dissemination ◽  
The Central Nervous System

scholarly journals PS913 ROLE OF CHOROID PLEXUS STROMA IN TUMOUR CHEMORESISTANCE: A SANCTUARY FOR LEUKAEMIA CELLS IN THE CENTRAL NERVOUS SYSTEM

HemaSphere ◽  
2019 ◽  
Vol 3 (S1) ◽  
pp. 412
Author(s):  
L.M. Fernández-Sevilla ◽  
J. Valencia ◽  
M.A. Flores ◽  
A. Fraile-Ramos ◽  
E. Jiménez ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Choroid Plexus ◽  
The Central Nervous System

Myo-inositol transport in the central nervous system

1975 ◽  
Vol 228 (5) ◽  
pp. 1510-1518 ◽  
Author(s):  
R Spector ◽  
AV Lorenzo
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Choroid Plexus ◽  
Intraventricular Injection ◽  
Affinity Constant ◽  
Rapid Injection ◽  
The Central Nervous System

Free myo-inositol (inositol) transport into the cerebrospinal fluid (CSF), brain, and choroid plexus and out of the cerebrospinal fluid was measured in rabbits. In vivo, inositol transport from blood into choroid plexus, CSF, and brain was saturable with an apparent affinity constant (K-t) of approximately 0.1 mM. The relative turnover of free inositol in choroid plexus (16 percent/h) was higher than in CSF 4percent/h) and brain (0.3percent/h) when meausred by tissue penetration of tracer [3-H]-labeled inositol injected into blood. However, the passage of tracer inositol was not greater than the passage of mannitol into brain when measured 15 s after a rapid injection of inositol and mannitol into the left common carotid artery. From the CSF, the clearance of inositol relative to inulin was saturable after the intraventricular injection of various concentrations of inositol and inulin. Moreover, a portion of the inositol cleared from the CSF entered brain by a saturable mechanism. In vitro, choroid plexuses, isolated from rabbits and incubated in artificial CSF, accumulated [3-H-labeled myo-inositol against a concentration gradient by a specific, active, saturable process with a K-t of 0.2 mM inositol. These results were interpreted as showing that the entry of inositol into the central nervous system from blood is regulated by a saturable transport system, and that the locus of this system may be, in part, in the choroid plexus.

scholarly journals Compartmentalization of HIV-1 in the central nervous system: role of the choroid plexus

AIDS ◽  
2005 ◽  
Vol 19 (7) ◽  
pp. 675-684 ◽  
Author(s):  
Evan J Burkala ◽  
Jun He ◽  
John T West ◽  
Charles Wood ◽  
Carol K Petito
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Choroid Plexus ◽  
The Central Nervous System ◽  
Hiv 1

scholarly journals Extramedullary Hematopoiesis in the Choroid Plexus of Five Dogs

1995 ◽  
Vol 32 (4) ◽  
pp. 437-440 ◽  
Author(s):  
D. Bienzle ◽  
J. M. Kwiecien ◽  
J. M. Parent
Keyword(s):  
Central Nervous System ◽  
Bone Marrow ◽  
Nervous System ◽  
Choroid Plexus ◽  
Fourth Ventricle ◽  
Extramedullary Hematopoiesis ◽  
Vascular Supply ◽  
The Other ◽  
The Central Nervous System ◽  
Refractory Seizures

Five dogs euthanatized because of refractory seizures were found to have hematopoietic elements in the interstitium of the choroid plexus at the level of the fourth ventricle. None of the dogs had significant hematologic or cerebrospinal fluid abnormalities. The extramedullary hematopoiesis was confined to the central nervous system and consisted of megakaryocytes, immature granulocytes, and rubricytes in two dogs and of one predominant cell population in each of the other three dogs. These findings are unique, and factors possibly contributing to the formation of a hematopoietic inductive microenvironment in the choroid plexus are cytokine-neurokine homologies, locally altered vascular supply, and aberrant functioning of bone marrow-derived central nervous system macrophages.

Extravascular foci ofTrypanosoma vivaxin goats: the central nervous system and aqueous humor of the eye as potential sources of relapse infections after chemotherapy

Parasitology ◽  
1988 ◽  
Vol 97 (1) ◽  
pp. 51-61 ◽  
Author(s):  
D. D. Whitelaw ◽  
P. R. Gardiner ◽  
M. Murray
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Choroid Plexus ◽  
Aqueous Humor ◽  
Acute Infection ◽  
Clinical Signs ◽  
Central Nervous System Involvement ◽  
Severe Illness ◽  
Diminazene Aceturate ◽  
The Central Nervous System

SUMMARYRelapse of parasitaemia after drug treatment of trypanosome infections is normally attributed to drug-resistance on the part of the parasite, under-dosage of the drug or reinfection of the host. In addition, inaccessibility of parasites to drug through sequestration in privileged extravascular sites has been shown in the past to occur withTrypanosoma brucei, and we have obtained evidence that extravascular foci ofT. vivaxcan also serve as a source of relapsing infections. Infection of goats with a West African stock ofT. vivaxresulted in severe illness, which was fatal if untreated. During the terminal stage of an acute infection, clinical signs of central nervous system involvement were apparent. Histologically, the choroid plexus was swollen and oedematous, and in some cases meningitis or meningoencephalitis was seen. Trypanosomes could be detected in the cerebrospinal fluid, and also extravascularly in the choroid plexus and meninges. In three cases they were present in the aqueous humor, associated with corneal cloudiness or opacity. Treatment of 2 goats with the trypanocidal drug diminazene aceturate eliminated parasitaemia, but infections in both relapsed about 6 weeks later, despite trypanosomes being undetectable in the bloodstream during the intervening period. We conclude that the relapse infections were caused by re-emergence of trypanosomes from the CNS and/or the eye, where sequestered parasites may have been inaccessible to the trypanocide.

scholarly journals Investigating the effects of novel heparan sulfate mimetic 'HS16-35' on immune cell migration in an in vitro model of the blood-CSF barrier.

2021 ◽  
Author(s):  
◽  
Maddie Griffiths
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Heparan Sulfate ◽  
Choroid Plexus ◽  
Immune Cells ◽  
Low Dose ◽  
Interferon Γ ◽  
The Central Nervous System

<p><b>The central nervous system was traditionally considered an immune-privileged site, defined as being immunologically inactive. However, recent studies have elucidated that a number of immune cells traffic into and out of the brain in healthy humans to conduct routine immunosurveillance. A unique immunological interface, the choroid plexus, acts as a gatekeeper for the entry of these immune cells during homeostasis. Although the mechanisms are not well described, the choroid plexus also has the capacity to regulate the responses of migrating leukocytes during inflammation.</b></p> <p>Multiple sclerosis is a complex neuroinflammatory disease characterized by demyelination in the CNS. Autoreactive immune cells invade the central nervous system and orchestrate an attack against myelin sheathes, the insulation layer that protects neurons. The disease affects nearly 1 in 1,000 New Zealanders, and currently has no cure. The most successful treatments for multiple sclerosis target the initial stages by inhibiting the entry of these cells into the central nervous system, however these are often associated with severe side and life-threatening effects and cannot prevent the progression of the disease.</p> <p>Heparanase, the ubiquitously expresses heparan sulfate degrading enzyme has been thoroughly implicated in the disease processes of multiple sclerosis, and its animal model, EAE. Autoreactive lymphocytes exploit heparanase activity to degrade the extracellular matrix and destabilize the barriers that maintain the relative immune privileged status of the central nervous system. Exogenous heparan sulfate mimetics have previously been shown to ameliorate symptoms of EAE by interfering with heparanase activity. However, the commercialization and clinical translation of these inhibitors is currently inhibited by the complexity of their synthesis. ‘HS16-35’ is a novel heparan sulfate mimetic developed by the Ferrier Institute, comprised of a dendritic core with four heavily sulfated oligosaccharide arms. The synthesis of this compound is much shorter due to its smaller size; however, it has been shown to act similarly to native heparan sulfate molecules. We proposed that HS16-35 is protective in preventing the migration of autoreactive immune cells across the choroid plexus by inhibiting lymphocyte heparanase.</p> <p>To investigate the efficacy of HS16-35 in vitro, we first established an experimental transwell model of the choroid plexus. This model incorporated core components of the choroid plexus, including fenestrated capillaries, the stromal matrix and epithelial monolayer. We first showed that the model was capable of mimicking homeostatic trafficking across the choroid plexus epithelium, which formed a selective but permeable barrier. Then, we induced T-cell specific inflammatory migration using Concanavalin A or TH1-type cytokines. This migration was found to be interferon-γ dependent and could be mitigated with anti-interferon-γ treatment.</p> <p>Once this model was established, we next investigated whether HS16-35 was effective in inhibiting inflammatory migration across this structure. To adapt HS16-35 to an in vitro dose, we performed cell viability assays. This confirmed that the compound was mildly cytotoxic to epithelial choroid plexus cells but not murine splenocytes. Further experiments found that low-dose HS16-35 did not impact monolayer permeability. Transwell migration assays showed that low-dose HS16-35 was effective in reducing ConA and interferon-γ mediated inflammatory T-cell migration to a level comparable to homeostatic trafficking. Finally, we assessed cytokine profiles of leukocytes and epithelial choroid plexus cells treated with HS16 35 and found that HS16-35 reduced the expression of key cytokines involved in MS pathogenesis.</p> <p>In summary, the work described in this thesis shows how HS16-35 may be protective during EAE by suppressing the inflammatory response of autoreactive T-cells, in addition to regulating the infiltration of immune cells into the CNS through the choroid plexus. In a broader sense, these findings show that HS16 36 may be effective in treating MS by regulating, not inhibiting lymphocyte migration into the CNS, mitigating some of the severe side effects that other migration-inhibitors face.</p>

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