Characterization of intracellular amyloid fibrils in the human choroid plexus epithelial cells

1990 ◽  
Vol 80 (6) ◽  
pp. 597-603 ◽  
Author(s):  
L. Eriksson ◽  
P. Westermark
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
Amyloid Fibrils ◽  
Human Choroid Plexus ◽  
Choroid Plexus Epithelial

Characterization of epithelial V-like antigen in human choroid plexus epithelial cells: Potential role in CNS immune surveillance

2011 ◽  
Vol 495 (2) ◽  
pp. 115-120 ◽  
Author(s):  
Elise Wojcik ◽  
Lisette M. Carrithers ◽  
Michael D. Carrithers
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
Potential Role ◽  
Immune Surveillance ◽  
Human Choroid Plexus ◽  
Choroid Plexus Epithelial

Mitogen-activated protein kinases are required for effective infection of human choroid plexus epithelial cells by Listeria monocytogenes

2017 ◽  
Vol 19 (1) ◽  
pp. 18-33 ◽  
Author(s):  
Stefanie Dinner ◽  
Julian Kaltschmidt ◽  
Carolin Stump-Guthier ◽  
Svetlana Hetjens ◽  
Hiroshi Ishikawa ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Epithelial Cells ◽  
Choroid Plexus ◽  
Protein Kinases ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Human Choroid Plexus ◽  
Choroid Plexus Epithelial

scholarly journals Characterization of folate uptake by choroid plexus epithelial cells in a rat primary culture model

2007 ◽  
Vol 104 (6) ◽  
pp. 1494-1503 ◽  
Author(s):  
Jan B. Wollack ◽  
Benedette Makori ◽  
Stuti Ahlawat ◽  
Rajeth Koneru ◽  
Sonia C. Picinich ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Culture ◽  
Choroid Plexus ◽  
Culture Model ◽  
Choroid Plexus Epithelial

scholarly journals Preterm Intraventricular Hemorrhage-Induced Inflammatory Response in Human Choroid Plexus Epithelial Cells

2021 ◽  
Vol 22 (16) ◽  
pp. 8648
Author(s):  
Zsolt Fejes ◽  
Marianna Pócsi ◽  
Jun Takai ◽  
Judit Erdei ◽  
Andrea Tóth ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Choroid Plexus ◽  
Adhesion Molecules ◽  
Intraventricular Hemorrhage ◽  
Cell Phenotype ◽  
Multiple Time ◽  
Mrna Levels ◽  
Human Choroid Plexus ◽  
Choroid Plexus Epithelial

Following an intraventricular hemorrhage (IVH), red blood cell lysis and hemoglobin (Hb) oxidation with the release of heme can cause sterile neuroinflammation. In this study, we measured Hb derivates and cellular adhesion molecules ICAM-1 and VCAM-1 with cell-free miRNAs in cerebrospinal fluid (CSF) samples obtained from Grade-III and Grade-IV preterm IVH infants (IVH-III and IVH-IV, respectively) at multiple time points between days 0–60 after the onset of IVH. Furthermore, human choroid plexus epithelial cells (HCPEpiCs) were incubated with IVH and non-IVH CSF (10 v/v %) for 24 h in vitro to investigate the IVH-induced inflammatory response that was investigated via: (i) HMOX1, IL8, VCAM1, and ICAM1 mRNAs as well as miR-155, miR-223, and miR-181b levels by RT-qPCR; (ii) nuclear translocation of the NF-κB p65 subunit by fluorescence microscopy; and (iii) reactive oxygen species (ROS) measurement. We found a time-dependent alteration of heme, IL-8, and adhesion molecules which revealed a prolonged elevation in IVH-IV vs. IVH-III with higher miR-155 and miR-181b expression at days 41–60. Exposure of HCPEpiCs to IVH CSF samples induced HMOX1, IL8, and ICAM1 mRNA levels along with increased ROS production via the NF-κB pathway activation but without cell death, as confirmed by the cell viability assay. Additionally, the enhanced intracellular miR-155 level was accompanied by lower miR-223 and miR-181b expression in HCPEpiCs after CSF treatment. Overall, choroid plexus epithelial cells exhibit an abnormal cell phenotype after interaction with pro-inflammatory CSF of IVH origin which may contribute to the development of later clinical complications in preterm IVH.

scholarly journals Susceptibility of Primary Human Choroid Plexus Epithelial Cells and Meningeal Cells to Infection by JC Virus

2018 ◽  
Vol 92 (8) ◽  
pp. e00105-18 ◽  
Author(s):  
Bethany A. O'Hara ◽  
Gretchen V. Gee ◽  
Walter J. Atwood ◽  
Sheila A. Haley
Keyword(s):  
Central Nervous System ◽  
Epithelial Cells ◽  
Choroid Plexus ◽  
Human Population ◽  
Brain Parenchyma ◽  
Wild Type ◽  
Meningeal Cells ◽  
Sialic Acid Binding ◽  
Human Choroid Plexus ◽  
Choroid Plexus Epithelial

ABSTRACTJC polyomavirus (JCPyV) establishes a lifelong persistence in roughly half the human population worldwide. The cells and tissues that harbor persistent virusin vivoare not known, but renal tubules and other urogenital epithelial cells are likely candidates as virus is shed in the urine of healthy individuals. In an immunosuppressed host, JCPyV can become reactivated and cause progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease of the central nervous system. Recent observations indicate that JCPyV may productively interact with cells in the choroid plexus and leptomeninges. To further study JCPyV infection in these cells, primary human choroid plexus epithelial cells and meningeal cells were challenged with virus, and their susceptibility to infection was compared to the human glial cell line, SVG-A. We found that JCPyV productively infects both choroid plexus epithelial cells and meningeal cellsin vitro. Competition with the soluble receptor fragment LSTc reduced virus infection in these cells. Treatment of cells with neuraminidase also inhibited both viral infection and binding. Treatment with the serotonin receptor antagonist, ritanserin, reduced infection in SVG-A and meningeal cells. We also compared the ability of wild-type and sialic acid-binding mutant pseudoviruses to transduce these cells. Wild-type pseudovirus readily transduced all three cell types, but pseudoviruses harboring mutations in the sialic acid-binding pocket of the virus failed to transduce the cells. These data establish a novel role for choroid plexus and meninges in harboring virus that likely contributes not only to meningoencephalopathies but also to PML.IMPORTANCEJCPyV infects greater than half the human population worldwide and causes central nervous system disease in patients with weakened immune systems. Several recent reports have found JCPyV in the choroid plexus and leptomeninges of patients with encephalitis. Due to their role in forming the blood-cerebrospinal fluid barrier, the choroid plexus and leptomeninges are also poised to play roles in virus invasion of brain parenchyma, where infection of macroglial cells leads to the development of progressive multifocal leukoencephalopathy, a severely debilitating and often fatal infection. In this paper we show for the first time that primary choroid plexus epithelial cells and meningeal cells are infected by JCPyV, lending support to the association of JCPyV with meningoencephalopathies. These data also suggest that JCPyV could use these cells as reservoirs for the subsequent invasion of brain parenchyma.

scholarly journals The Lyme disease bacterium, Borrelia burgdorferi, stimulates an inflammatory response in human choroid plexus epithelial cells

PLoS ONE ◽  
2020 ◽  
Vol 15 (7) ◽  
pp. e0234993 ◽  
Author(s):  
Derick Thompson ◽  
Jordyn Sorenson ◽  
Jacob Greenmyer ◽  
Catherine A. Brissette ◽  
John A. Watt
Keyword(s):  
Lyme Disease ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Borrelia Burgdorferi ◽  
Choroid Plexus ◽  
Human Choroid Plexus ◽  
Choroid Plexus Epithelial

scholarly journals Porcine Choroid Plexus Epithelial Cells Induce Streptococcus suis Bacteriostasis In Vitro

2004 ◽  
Vol 72 (5) ◽  
pp. 3084-3087 ◽  
Author(s):  
Rüdiger A. Adam ◽  
Tobias Tenenbaum ◽  
Peter Valentin-Weigand ◽  
Maurice Laryea ◽  
Bernd Schwahn ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bacterial Meningitis ◽  
Choroid Plexus ◽  
Host Defense ◽  
Streptococcus Suis ◽  
Active Role ◽  
Necrosis Factor Alpha ◽  
Ifn Γ ◽  
Choroid Plexus Epithelial

ABSTRACT The involvement of the choroid plexus in host defense during bacterial meningitis is unclear. Aiming to elucidate possible antibacterial mechanisms, we stimulated primary porcine choroid plexus epithelial cells (pCPEC) with proinflammatory cytokines and challenged them with various Streptococcus suis strains. In the supernatant of gamma interferon (IFN-γ)-stimulated pCPEC, streptococcal growth was markedly suppressed. Costimulation with tumor necrosis factor alpha enhanced this bacteriostatic effect, while supplementation of l-tryptophan completely eliminated it. We also demonstrate that an activation of indoleamine 2,3-dioxygenase in the pCPEC seems to be responsible for the IFN-γ-induced bacteriostasis. This supports the hypothesis of an active role of the choroid plexus in host defense against bacterial meningitis.

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