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 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 Walnut Oil Alleviates Intestinal Inflammation and Restores Intestinal Barrier Function in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1302
Author(s):  
Adrian Bartoszek ◽  
Adam Makaro ◽  
Agnieszka Bartoszek ◽  
Radzisław Kordek ◽  
Jakub Fichna ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dietary Habits ◽  
Intestinal Inflammation ◽  
Visceral Pain ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Walnut Oil ◽  
Wide Range ◽  
Bowel Diseases ◽  
Anti Inflammatory

Ulcerative colitis belongs to inflammatory bowel diseases, which is a group of chronic disorders of the gastrointestinal tract. It is a debilitating condition with a wide range of symptoms including rectal bleeding, diarrhea, and visceral pain. Current dietary habits often lead to imbalance in n-6/n-3 polyunsaturated fatty acids (PUFA) in favor of n-6 PUFA. Recent data showed the potential anti-inflammatory advantage of n-3 PUFA. Walnut oil (WO) is rich in those fatty acids and mainly consists of linoleic and linolenic acids that may act via free fatty acids receptors (FFARs). We assessed the anti-inflammatory effect of WO in the mouse model of dextran sulfate sodium (DSS)-induced colitis. Moreover, we examined changes in the expression of tight junction proteins (TJ), pro-inflammatory cytokines, and FFAR proteins in the inflamed mouse colon. WO improves the damage score in inflamed tissue, significantly restoring ion transport and colonic wall permeability. Inflammation caused changes in TJ, FFAR, and pro-inflammatory gene proteins expression, which WO was able to partially reverse. WO has anti-inflammatory properties; however, its exact mechanism of action remains unclear. This stems from the pleiotropic effects of n-3 PUFA ligands associated with receptor distribution and targeted signaling pathways.

scholarly journals The long-term consequences of antibiotic therapy: Role of colonic short-chain fatty acids (SCFA) system and intestinal barrier integrity

PLoS ONE ◽  
2019 ◽  
Vol 14 (8) ◽  
pp. e0220642 ◽  
Author(s):  
Yuliia Holota ◽  
Taisa Dovbynchuk ◽  
Izumi Kaji ◽  
Igor Vareniuk ◽  
Natalia Dzyubenko ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Antibiotic Therapy ◽  
Intestinal Barrier ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Barrier Integrity ◽  
Intestinal Barrier Integrity ◽  
Long Term Consequences

scholarly journals Fatty acids from diet and microbiota regulate energy metabolism

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 738 ◽  
Author(s):  
Joe Alcock ◽  
Henry C. Lin
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Gut Microbiota ◽  
Barrier Function ◽  
Unsaturated Fatty Acids ◽  
Intestinal Barrier ◽  
Dietary Fats ◽  
Intestinal Barrier Function ◽  
Metabolic Endotoxemia

A high-fat diet and elevated levels of free fatty acids are known risk factors for metabolic syndrome, insulin resistance, and visceral obesity. Although these disease associations are well established, it is unclear how different dietary fats change the risk of insulin resistance and metabolic syndrome. Here, we review emerging evidence that insulin resistance and fat storage are linked to changes in the gut microbiota. The gut microbiota and intestinal barrier function, in turn, are highly influenced by the composition of fat in the diet. We review findings that certain fats (for example, long-chain saturated fatty acids) are associated with dysbiosis, impairment of intestinal barrier function, and metabolic endotoxemia. In contrast, other fatty acids, including short-chain and certain unsaturated fatty acids, protect against dysbiosis and impairment of barrier function caused by other dietary fats. These fats may promote insulin sensitivity by inhibiting metabolic endotoxemia and dysbiosis-driven inflammation. During dysbiosis, the modulation of metabolism by diet and microbiota may represent an adaptive process that compensates for the increased fuel demands of an activated immune system.

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.

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