scholarly journals Food Contaminants Effects on an In Vitro Model of Human Intestinal Epithelium

Toxics ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 135
Author(s):  
Marion Guibourdenche ◽  
Johanna Haug ◽  
Noëllie Chevalier ◽  
Madeleine Spatz ◽  
Nicolas Barbezier ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intestinal Permeability ◽  
Intestinal Epithelium ◽  
In Vitro Model ◽  
Food Contaminants ◽  
Gut Barrier ◽  
Gut Barrier Function ◽  
Vitro Model ◽  
Human Intestinal Epithelium

Pesticide residues represent an important category of food contaminants. Furthermore, during food processing, some advanced glycation end-products resulting from the Maillard reaction can be formed. They may have adverse health effects, in particular on the digestive tract function, alone and combined. We sought to validate an in vitro model of the human intestinal barrier to mimic the effects of these food contaminants on the epithelium. A co-culture of Caco-2/TC7 cells and HT29-MTX was stimulated for 6 h with chlorpyrifos (300 μM), acrylamide (5 mM), Nε-Carboxymethyllysine (300 μM) alone or in cocktail with a mix of pro-inflammatory cytokines. The effects of those contaminants on the integrity of the gut barrier and the inflammatory response were analyzed. Since the co-culture responded to inflammatory stimulation, we investigated whether this model could be used to evaluate the effects of food contaminants on the human intestinal epithelium. CPF alone affected tight junctions’ gene expression, without inducing any inflammation or alteration of intestinal permeability. CML and acrylamide decreased mucins gene expression in the intestinal mucosa, but did not affect paracellular intestinal permeability. CML exposure activated the gene expression of MAPK pathways. The co-culture response was stable over time. This cocktail of food contaminants may thus alter the gut barrier function.

Anti-inflammatory effects of dietary phenolic compounds in an in vitro model of inflamed human intestinal epithelium

2010 ◽  
Vol 188 (3) ◽  
pp. 659-667 ◽  
Author(s):  
Thérèse Sergent ◽  
Neil Piront ◽  
Julie Meurice ◽  
Olivier Toussaint ◽  
Yves-Jacques Schneider
Keyword(s):  
Phenolic Compounds ◽  
Intestinal Epithelium ◽  
In Vitro Model ◽  
Anti Inflammatory ◽  
Vitro Model ◽  
Human Intestinal Epithelium

scholarly journals Development of Physiologically Responsive Human iPSC-Derived Intestinal Epithelium to Study Barrier Dysfunction in IBD

2020 ◽  
Vol 21 (4) ◽  
pp. 1438 ◽  
Author(s):  
John P. Gleeson ◽  
Hannah Q. Estrada ◽  
Michifumi Yamashita ◽  
Clive N. Svendsen ◽  
Stephan R. Targan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intestinal Permeability ◽  
Intestinal Epithelium ◽  
Adherens Junction ◽  
Induced Pluripotent Stem Cell ◽  
Barrier Dysfunction ◽  
Junction Protein ◽  
Vitro Model ◽  
Induced Pluripotent

In inflammatory bowel disease (IBD), the intestinal epithelium is characterized by increased permeability both in active disease and remission states. The genetic underpinnings of this increased intestinal permeability are largely unstudied, in part due to a lack of appropriate modelling systems. Our aim is to develop an in vitro model of intestinal permeability using induced pluripotent stem cell (iPSC)-derived human intestinal organoids (HIOs) and human colonic organoids (HCOs) to study barrier dysfunction. iPSCs were generated from healthy controls, adult onset IBD, and very early onset IBD (VEO-IBD) patients and differentiated into HIOs and HCOs. EpCAM+ selected cells were seeded onto Transwell inserts and barrier integrity studies were carried out in the presence or absence of pro-inflammatory cytokines TNFα and IFNγ. Quantitative real-time PCR (qRT-PCR), transmission electron microscopy (TEM), and immunofluorescence were used to determine altered tight and adherens junction protein expression or localization. Differentiation to HCO indicated an increased gene expression of CDX2, CD147, and CA2, and increased basal transepithelial electrical resistance compared to HIO. Permeability studies were carried out in HIO- and HCO-derived epithelium, and permeability of FD4 was significantly increased when exposed to TNFα and IFNγ. TEM and immunofluorescence imaging indicated a mislocalization of E-cadherin and ZO-1 in TNFα and IFNγ challenged organoids with a corresponding decrease in mRNA expression. Comparisons between HIO- and HCO-epithelium show a difference in gene expression, electrophysiology, and morphology: both are responsive to TNFα and IFNγ stimulation resulting in enhanced permeability, and changes in tight and adherens junction architecture. This data indicate that iPSC-derived HIOs and HCOs constitute an appropriate physiologically responsive model to study barrier dysfunction and the role of the epithelium in IBD and VEO-IBD.

Comparing Toxicity of Alumina and Zinc Oxide Nanoparticles on the Human Intestinal Epithelium In Vitro Model

2017 ◽  
Vol 17 (5) ◽  
pp. 2881-2891 ◽  
Author(s):  
Zheng-Mei Song ◽  
Huan Tang ◽  
Xiaoyong Deng ◽  
Kun Xiang ◽  
Aoneng Cao ◽  
...  
Keyword(s):  
Zinc Oxide ◽  
Intestinal Epithelium ◽  
Zinc Oxide Nanoparticles ◽  
In Vitro Model ◽  
Oxide Nanoparticles ◽  
Vitro Model ◽  
Human Intestinal Epithelium

scholarly journals Morphofunctional properties of a differentiated Caco2/HT-29 co-culture as an in vitro model of human intestinal epithelium

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Anita Ferraretto ◽  
Michela Bottani ◽  
Paola De Luca ◽  
Laura Cornaghi ◽  
Francesca Arnaboldi ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
In Vitro Model ◽  
Transepithelial Transport ◽  
Intestinal Cell ◽  
Blue Staining ◽  
Alcian Blue Staining ◽  
Vitro Model ◽  
Human Intestinal Epithelium ◽  
Ht 29

An intestinal 70/30 Caco2/HT-29 co-culture was set up starting from the parental populations of differentiated cells to mimic the human intestinal epithelium. Co-culture was harvested at confluence 0 (T0) and at 3, 6, 10, and 14 days post confluence after plating (T3, T6, T10, and T14, respectively) for morphological and functional analysis. Transmission electron microscopy revealed different features from T0 to T14: microvilli and a complete junctional apparatus from T6, mucus granules from T3, as also confirmed by PAS/Alcian Blue staining. The specific activity of alkaline phosphatase (ALP), aminopeptidase N (APN), and dipeptidyl peptidase IV (DPPIV) progressively increased after T0, indicating the acquirement of a differentiated and digestive phenotype. Transepithelial electrical resistance (TEER), indicative of the barrier properties of the monolayer, increased from T0 up to T6 reaching values very similar to the human small intestine. The apparent permeability coefficient for Lucifer Yellow (LY), along with morphological analysis, reveals a good status of the tight junctions. At T14, HT-29 cells reduced to 18.4% and formed domes, indicative of transepithelial transport of nutrients. This Caco2/HT-29 co-culture could be considered a versatile and suitable in vitro model of human intestinal epithelium for the presence of more than one prevalent intestinal cell type, by means of a minimum of 6 to a maximum of 14 post-confluence days obtained without the need of particular inducers of subclones and growth support to reach an intestinal differentiated phenotype.

Anti-inflammatory properties of fruit juices enriched with pine bark extract in an in vitro model of inflamed human intestinal epithelium: The effect of gastrointestinal digestion

2013 ◽  
Vol 53 ◽  
pp. 94-99 ◽  
Author(s):  
Carmen Frontela-Saseta ◽  
Rubén López-Nicolás ◽  
Carlos A. González-Bermúdez ◽  
Carmen Martínez-Graciá ◽  
Gaspar Ros-Berruezo
Keyword(s):  
Intestinal Epithelium ◽  
In Vitro Model ◽  
Fruit Juices ◽  
Pine Bark ◽  
Bark Extract ◽  
Gastrointestinal Digestion ◽  
Anti Inflammatory ◽  
Vitro Model ◽  
Human Intestinal Epithelium

scholarly journals Pulmonary fibroblasts: an in vitro model of emphysema. Regulation of elastin gene expression.

1990 ◽  
Vol 265 (26) ◽  
pp. 15544-15549 ◽  
Author(s):  
J.A. Foster ◽  
C.B. Rich ◽  
M.F. Miller
Keyword(s):  
Gene Expression ◽  
In Vitro Model ◽  
Pulmonary Fibroblasts ◽  
Vitro Model ◽  
Elastin Gene
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