In vitro-model for Toxoplasma gondii invasion into neuroepithelial cells

1998 ◽  
Vol 180 (4) ◽  
pp. 299-305 ◽  
Author(s):  
Bodo Kurz ◽  
Wolfgang Böckeler ◽  
Eberhard Buse
Keyword(s):  
Toxoplasma Gondii ◽  
In Vitro Model ◽  
Neuroepithelial Cells ◽  
Vitro Model

scholarly journals Preterm Intraventricular Hemorrhage in vitro: Modeling the Cytopathology of the Ventricular Zone

2020 ◽  
Author(s):  
Leandro Castaneyra-Ruiz ◽  
James P. McAllister ◽  
Diego M. Morales ◽  
Steven L. Brody ◽  
Albert M. Isaacs ◽  
...  
Keyword(s):  
Intraventricular Hemorrhage ◽  
In Vitro Model ◽  
Ependymal Cell ◽  
Ventricular Zone ◽  
High Temporal Resolution ◽  
Neuroepithelial Cells ◽  
Vitro Model ◽  
Developmental Features ◽  
The Impact

Abstract Background: Severe intraventricular hemorrhage (IVH) is one of the most devastating neurological complications in preterm infants, with the majority suffering long-term neurological morbidity and up to 50 percent developing post hemorrhagic hydrocephalus (PHH). Despite the importance of this disease, its cytopathological mechanisms are not well known. An in vitro model of IVH is required to investigate the effects of blood and its components on the developing ventricular zone (VZ) and its stem cell niche. To address this need, we developed a new in vitro model to mimic the cytopathological conditions of IVH in the preterm infant. Methods: Maturing neuroepithelial cells from the VZ were harvested from the entire lateral ventricles of wild type C57BL/6 mice at 1-4 days of age and expanded in proliferation media for 3-5 days. At confluence, cells were re-plated onto 24-well plates in differentiation media to generate ependymal cells (EC). At approximately 3-5 days, which corresponded to the onset of ependymal cell differentiation based on the appearance of multiciliated cells , phosphate-buffered saline for controls or syngeneic whole blood for IVH was added to the ependymal cell surface. The cells were examined for the expression of EC markers of differentiation and maturation to qualitatively and quantitatively assess the effect of blood exposure on VZ transition from neuroepithelial cells to EC. Discussion: This model will allow investigators to test cytopathological mechanisms contributing to the pathology of IVH with high temporal resolution and query the impact of injury to the maturation of the VZ. This technique recapitulates features of normal maturation of the VZ in vitro, offering the capacity to investigate the developmental features of VZ biogenesis.

The in vitro model of tissue cyst formation in Toxoplasma gondii

1994 ◽  
Vol 10 (7) ◽  
pp. 281-285 ◽  
Author(s):  
T.D. McHugh ◽  
R.E. Holliman ◽  
P.D. Butcher
Keyword(s):  
Toxoplasma Gondii ◽  
In Vitro Model ◽  
Cyst Formation ◽  
Tissue Cyst ◽  
Vitro Model

scholarly journals Preterm intraventricular hemorrhage in vitro: modeling the cytopathology of the ventricular zone

2020 ◽  
Author(s):  
Leandro Castaneyra-Ruiz ◽  
James P. McAllister ◽  
Diego M. Morales ◽  
Steven L. Brody ◽  
Albert M. Isaacs ◽  
...  
Keyword(s):  
Intraventricular Hemorrhage ◽  
In Vitro Model ◽  
Ventricular Zone ◽  
Ependymal Cells ◽  
High Temporal Resolution ◽  
Neuroepithelial Cells ◽  
Vitro Model ◽  
Developmental Features ◽  
The Impact

Abstract Background: Severe intraventricular hemorrhage (IVH) is one of the most devastating neurological complications in preterm infants, with the majority suffering long-term neurological morbidity and up to 50 percent developing post-hemorrhagic hydrocephalus (PHH). Despite the importance of this disease, its cytopathological mechanisms are not well known. An in vitro model of IVH is required to investigate the effects of blood and its components on the developing ventricular zone (VZ) and its stem cell niche. To address this need, we developed a protocol from our accepted in vitro model to mimic the cytopathological conditions of IVH in the preterm infant. Methods: Maturing neuroepithelial cells from the VZ were harvested from the entire lateral ventricles of wild type C57BL/6 mice at 1-4 days of age and expanded in proliferation media for 3-5 days. At confluence, cells were re-plated onto 24-well plates in differentiation media to generate ependymal cells (EC). At approximately 3-5 days, which corresponded to the onset of EC differentiation based on the appearance of multiciliated cells, phosphate-buffered saline for controls or syngeneic whole blood for IVH was added to the EC surface. The cells were examined for the expression of EC markers of differentiation and maturation to qualitatively and quantitatively assess the effect of blood exposure on VZ transition from neuroepithelial cells to EC. Discussion: This protocol will allow investigators to test cytopathological mechanisms contributing to the pathology of IVH with high temporal resolution and query the impact of injury to the maturation of the VZ. This technique recapitulates features of normal maturation of the VZ in vitro, offering the capacity to investigate the developmental features of VZ biogenesis.

scholarly journals Primary brain cell infection by Toxoplasma gondii reveals the extent and dynamics of parasite differentiation and impact on neuron biology.

2021 ◽  
Author(s):  
Thomas Mouveaux ◽  
Emmanuel Roger ◽  
Alioune Gueye ◽  
Fanny Eysert ◽  
Ludovic Huot ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
In Vitro Model ◽  
Brain Cell ◽  
Brain Cells ◽  
Specific Response ◽  
Cell Infection ◽  
Vitro Model ◽  
The Brain

Toxoplasma gondii is a eukaryotic parasite that form latent cyst in the brain of immunocompetent individuals. The latent parasites infection of the immune privileged central nervous system is linked to most complications. With no drug currently available to eliminate the latent cysts in the brain of infected hosts, the consequences of neurons long-term infection are unknown. It has long been known that T. gondii specifically differentiate into a latent form (bradyzoite) in neurons, but how the infected neuron is responding to the infection remain to be elucidated. We have established a new in vitro model resulting in the production of fully mature bradyzoites cysts in brain cells. Using dual, host and parasite, RNA-seq we characterized the dynamics of differentiation of the parasite, revealing the involvement of key pathways in this process. Moreover, we identified how the infected brain cells responded to the parasite infection revealing the drastic changes that take place. We showed that neuronal specific pathways are strongly affected, with synapse signaling being particularly affected, especially glutamatergic synapse. The establishment of this new in vitro model allows to investigate both the dynamics of the parasite differentiation and the specific response of neurons to the long term infection by this parasite.

scholarly journals Preterm Intraventricular Hemorrhage in vitro: Modeling the Cytopathology of the Ventricular Zone

2020 ◽  
Author(s):  
Leandro Castaneyra-Ruiz ◽  
James P. McAllister ◽  
Diego M. Morales ◽  
Steven L. Brody ◽  
Albert M. Isaacs ◽  
...  
Keyword(s):  
Intraventricular Hemorrhage ◽  
In Vitro Model ◽  
Ependymal Cell ◽  
Ventricular Zone ◽  
High Temporal Resolution ◽  
Neuroepithelial Cells ◽  
Vitro Model ◽  
Developmental Features ◽  
The Impact

Abstract Background: Severe intraventricular hemorrhage (IVH) is one of the most devastating neurological complications in preterm infants, with the majority suffering long-term neurological morbidity and up to 50 percent developing post hemorrhagic hydrocephalus (PHH). Despite the importance of this disease, its cytopathological mechanisms are not well known. An in vitro model of IVH is required to investigate the effects of blood and its components on the developing ventricular zone (VZ) and its stem cell niche. To address this need, we developed a new in vitro model to mimic the cytopathological conditions of IVH in the preterm infant. Methods: Maturing neuroepithelial cells from the VZ were harvested from the entire lateral ventricles of wild type C57BL/6 mice at 1-4 days of age and expanded in proliferation media for 3-5 days. At confluence, cells were re-plated onto 24-well plates in differentiation media to generate ependymal cells (EC). At approximately 3-5 days, which corresponded to the onset of ependymal cell differentiation based on the appearance of multiciliated cells , phosphate-buffered saline for controls or syngeneic whole blood for IVH was added to the ependymal cell surface. The cells were examined for the expression of EC markers of differentiation and maturation to qualitatively and quantitatively assess the effect of blood exposure on VZ transition from neuroepithelial cells to EC. Discussion: This model will allow investigators to test cytopathological mechanisms contributing to the pathology of IVH with high temporal resolution and query the impact of injury to the maturation of the VZ. This technique recapitulates features of normal maturation of the VZ in vitro, offering the capacity to investigate the developmental features of VZ biogenesis.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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