Stobadine attenuates impairment of an intestinal barrier model caused by 4-hydroxynonenal

2013 ◽  
Vol 27 (1) ◽  
pp. 426-432 ◽  
Author(s):  
Marina Cindric ◽  
Ana Cipak ◽  
Emilija Zapletal ◽  
Morana Jaganjac ◽  
Lidija Milkovic ◽  
...  
Keyword(s):  
Intestinal Barrier ◽  
Barrier Model

Cyanobacterial lipopeptides puwainaphycins and minutissamides induce disruptive and pro-inflammatory processes in Caco-2 human intestinal barrier model

Harmful Algae ◽  
2020 ◽  
Vol 96 ◽  
pp. 101849
Author(s):  
Ondřej Vašíček ◽  
Jan Hájek ◽  
Lucie Bláhová ◽  
Pavel Hrouzek ◽  
Pavel Babica ◽  
...  
Keyword(s):  
Intestinal Barrier ◽  
Inflammatory Processes ◽  
Barrier Model

scholarly journals Characterizing Phage-Host Interactions in a Simplified Human Intestinal Barrier Model

2020 ◽  
Vol 8 (9) ◽  
pp. 1374
Author(s):  
María A. Núñez-Sánchez ◽  
Joan Colom ◽  
Lauren Walsh ◽  
Colin Buttimer ◽  
Andrei Sorin Bolocan ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
In Vitro Model ◽  
Cell Model ◽  
Layer Structure ◽  
Intestinal Barrier ◽  
Host Interactions ◽  
Intestinal Epithelia ◽  
Vitro Model ◽  
Barrier Model

An intestinal epithelium model able to produce mucus was developed to provide an environment suitable for testing the therapeutic activity of gut bacteriophages. We show that Enterococcus faecalis adheres more effectively in the presence of mucus, can invade the intestinal epithelia and is able to translocate after damaging tight junctions. Furthermore, Enterococcus phage vB_EfaM_A2 (a member of Herelleviridae that possesses virion associated immunoglobin domains) was found to translocate through the epithelium in the presence and absence of its host bacteria. Phage A2 protected eukaryotic cells by reducing mortality and maintaining the structure of the cell layer structure. We suggest the mammalian cell model utilized within this study as an adaptable in vitro model that can be employed to enable a better understanding of phage–bacteria interactions and the protective impact of phage therapy relating to the intestinal epithelium.

scholarly journals Side‐Directed Transfer and Presystemic Metabolism of Selenoneine in a Human Intestinal Barrier Model

2019 ◽  
Vol 63 (12) ◽  
pp. 1900080 ◽  
Author(s):  
Isabelle Rohn ◽  
Nina Kroepfl ◽  
Julia Bornhorst ◽  
Doris Kuehnelt ◽  
Tanja Schwerdtle
Keyword(s):  
Intestinal Barrier ◽  
Presystemic Metabolism ◽  
Barrier Model

scholarly journals A novel two-compartment barrier model for investigating nanoparticle transport in fish intestinal epithelial cells

2016 ◽  
Vol 3 (2) ◽  
pp. 388-395 ◽  
Author(s):  
Mark Geppert ◽  
Laura Sigg ◽  
Kristin Schirmer
Keyword(s):  
Rainbow Trout ◽  
Epithelial Cells ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Intestinal Epithelial ◽  
Nanoparticle Transport ◽  
Barrier Model

We introduce a novel in vitro rainbow trout intestinal barrier model and demonstrate its suitability for investigating nanoparticle transport across the intestinal epithelium.

Human gut-on-a-chip model as an improved intestinal barrier model to predict compound bioavailability and toxicity

2018 ◽  
Vol 295 ◽  
pp. S73
Author(s):  
H. Bouwmeester ◽  
K. Kulthong ◽  
M. Grouls ◽  
L. Duivenvoorde ◽  
D. Rijkers ◽  
...  
Keyword(s):  
Intestinal Barrier ◽  
Human Gut ◽  
Barrier Model

Arsenic-containing hydrocarbons and arsenic-containing fatty acids: Transfer across and presystemic metabolism in the Caco-2 intestinal barrier model

2015 ◽  
Vol 59 (10) ◽  
pp. 2044-2056 ◽  
Author(s):  
Sören Meyer ◽  
Georg Raber ◽  
Franziska Ebert ◽  
Mojtaba S Taleshi ◽  
Kevin A Francesconi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Intestinal Barrier ◽  
Presystemic Metabolism ◽  
Barrier Model

scholarly journals Deoxycholic Acid Modulates Cell-Junction Gene Expression and Increases Intestinal Barrier Dysfunction in Caco-2 Cell Monolayers

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 956-956
Author(s):  
Huawei Zeng ◽  
Bryan Safratowich ◽  
Wen-Hsing Cheng ◽  
Kate Claycombe-Larson ◽  
Mary Briske-Anderson
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Bile Acids ◽  
Deoxycholic Acid ◽  
Intestinal Barrier ◽  
Cell Junction ◽  
Epithelial Barrier ◽  
Pcr Array ◽  
Barrier Dysfunction ◽  
Barrier Model

Abstract Objectives Diet-related obesity is associated with an increased risk of developing intestinal hyperpermeability. High dietary fat intake causes an increase in colonic bile acids (BAs), particularly deoxycholic acid (DCA, secondary BA), which may disrupt the intestinal epithelial barrier. To determine the potential role of bile acids in barrier dysfunction, we hypothesize that DCA modulates the gene expression in multiple cell junction pathways and increases intestinal permeability. Methods With a Caco-2 cell intestinal barrier model, we used cell proliferation, PCR array, biochemical, western blotting and immunofluorescent assays to examine the impact of DCA on the integrity of intestinal barrier and gene expression. Results Human intestinal Caco-2 cells were grown in monolayers and challenged with DCA at physiological concentrations (sub mM levels). DCA increased transcellular and paracellular permeability (>30%) via transepithelial electrical resistance and phenol red flux measurements. Similarly, DCA increased intracellular reactive oxidative species production (>1-fold) and accompanied a modification of cellular p38 and ERK1/2 signaling pathways. Further characterization of underlying genes related to epithelial barrier with PCR array analysis identified that 23 genes (in tight junction, focal adhesion, gap junction and adhere junction pathways) were decreased at least 40% in (0.25 mM) DCA-treated Caco-2 cells when compared to untreated cells. Finally, we demonstrated that DCA decreased the protein levels of occludin gene at both cellular tight junction and nucleus in epithelial cells. Conclusions Collectively, our data suggest that at physiological concentrations, DCA alters the gene expression of multiple pathways related to cell junctions and increases permeability in a Caco-2 intestinal barrier model. These molecular events may represent the underlying mechanistic pathways that are responsible for DCA-induced transcellular and paracellular permeation. Funding Sources This work was supported by U.S. Department of Agriculture, Agricultural Research Service, research project 3062-51,000-056–00D.

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