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.

scholarly journals Inhibition of HtrA2 alleviated colitis by preventing necroptosis of intestinal epithelial cells

2018 ◽  
Author(s):  
Chong Zhang ◽  
Andong He ◽  
Shuai Liu ◽  
Qiaoling He ◽  
Yiqin Luo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Rational Design ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Body Weight Loss ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial ◽  
Tandem Mass Tag ◽  
Function Loss

AbstractNecroptosis of intestinal epithelial cells has been indicated to play an important role in the pathogenesis of inflammatory bowel disease (IBD). The identification of dysregulated proteins that can regulate necroptosis in dextran sulfate sodium (DSS)-induced colitis is the key to the rational design of therapeutic strategies for colitis. Through Tandem Mass Tag (TMT)-based quantitative proteomics, HtrA2 was found to be downregulated in the colon of DSS-treated mice. UCF-101, a specific serine protease inhibitor of HtrA2, significantly alleviated DSS-induced colitis as indicated by prevention of body weight loss and decreased mortality. UCF-101 decreased DSS-induced colonic inflammation, prevented intestinal barrier function loss and inhibited necroptosis of intestinal epithelial cells. In vitro, UCF-101 or silencing of HtrA2 decreased necroptosis of HT-29 and L929 cells. UCF-101 decreased phosphorylation of RIPK1 and subsequent phosphorylation of RIPK3 and MLKL during necroptosis. HtrA2 directly interacted with RIPK1 and promoted its degradation during a specific time phase of necroptosis. Our findings highlight the importance of HtrA2 in regulating colitis by modulation of necroptosis and suggest HtrA2 as an attractive target for anti-colitis treatment.

scholarly journals Expression of Human Decay-Accelerating Factor on Intestinal Epithelium of Transgenic Mice Does Not Facilitate Infection by the Enteral Route

2015 ◽  
Vol 89 (8) ◽  
pp. 4311-4318 ◽  
Author(s):  
Jieyan Pan ◽  
Lili Zhang ◽  
Matthew A. Odenwald ◽  
Le Shen ◽  
Jerrold R. Turner ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Transgenic Mice ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cells ◽  
Apical Cell ◽  
Oral Route ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Cvb3 Infection

ABSTRACTIn vitro, infection of polarized human intestinal epithelial cells by coxsackievirus B3 (CVB3) depends on virus interaction with decay-accelerating factor (DAF), a receptor expressed on the apical cell surface. Although mice are highly susceptible to CVB3 infection when virus is delivered by intraperitoneal injection, infection by the enteral route is very inefficient. Murine DAF, unlike human DAF, does not bind virus, and we hypothesized that the absence of an accessible receptor on the intestinal surface is an important barrier to infection by the oral route. We generated transgenic mice that express human DAF specifically on intestinal epithelium and measured their susceptibility to infection by a DAF-binding CVB3 isolate. Human DAF permitted CVB3 to bind to the intestinal surfaceex vivoand to infect polarized monolayers of small-intestinal epithelial cells derived from DAF transgenic mice. However, expression of human DAF did not facilitate infection by the enteral route either in immunocompetent animals or in animals deficient in the interferon alpha/beta receptor. These results indicate that the absence of an apical receptor on intestinal epithelium is not the major barrier to infection of mice by the oral route.IMPORTANCECVB3 infection of human intestinal epithelial cells depends on DAF at the apical cell surface, and expression of human DAF on murine intestinal epithelial cells permits their infectionin vitro. However, expression of human DAF on the intestinal surface of transgenic mice did not facilitate infection by the oral route. Although the role of intestinal DAF in human infection has not been directly examined, these results suggest that DAF is not the critical factor in mice.

scholarly journals Aggregation Substance Increases Adherence and Internalization, but Not Translocation, of Enterococcus faecalisthrough Different Intestinal Epithelial Cells In Vitro

2000 ◽  
Vol 68 (10) ◽  
pp. 6044-6047 ◽  
Author(s):  
S. Sartingen ◽  
E. Rozdzinski ◽  
A. Muscholl-Silberhorn ◽  
R. Marre
Keyword(s):  
Epithelial Cells ◽  
Enterococcus Faecalis ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cells ◽  
Bacterial Adherence ◽  
Intestinal Epithelial ◽  
Aggregation Substance

ABSTRACT The aggregation substance of Enterococcus faecalisincreased bacterial adherence to and internalization by epithelial cells originating from the colon and duodenum but not by cells derived from the ileum. However, enterococcal translocation through monolayers of intestinal epithelium was not observed.

scholarly journals In vitro effect of uremic serum on barrier function and inflammation in human colonocytes

2018 ◽  
Vol 40 (3) ◽  
pp. 217-224 ◽  
Author(s):  
Laila Santos de Andrade ◽  
Maria Aparecida Dalboni ◽  
José Tarcisio Giffoni de Carvalho ◽  
Caren Cristina Grabulosa ◽  
Natalia Barros Ferreira Pereira ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Potential Effect ◽  
Intestinal Epithelial ◽  
T84 Cells ◽  
Uremic Serum ◽  
Inflammatory State ◽  
Vitro Effect

ABSTRACT Introduction: In chronic kidney disease (CKD), it has been suggested that alterations within the gut are associated with an inflammatory state and uremic toxicity. Studies suggest that uremia may impair the function of the intestinal barrier via the promotion of increased intestinal permeability. To understand the mechanisms that are involved in intestinal barrier damage in the setting of uremia, we evaluated the in vitro effect of uremic serum on transepithelial electrical resistance (TER), inflammation, and apoptosis in intestinal epithelial cells (T84). Methods: Pools of serum from healthy individuals, patients not on dialysis, and patients on hemodialysis (Pre-HD and Post-HD) were prepared. T84 cells were incubated for 24 h in medium, of which 10% consisted of the pooled serum from each group. After incubation, the TER was measured and the following parameters were determined by flow cytometry: expression of toll-like receptors (TLRs), production of reactive oxygen species (ROS), and apoptosis. The level of IL-6 in the culture supernatant was determined by ELISA. Results: No difference was observed among the groups with respect to TER, apoptosis, and ROS or the expression of TLR-2, TLR-4, and TLR-9. IL-6 secretion was higher (p < 0.001) in cells that were incubated with pre- and post-HD serum. Conclusion: The results that were obtained from this model suggest that uremic serum per se does not seem to impair the integrity of intestinal epithelial cells. The increased IL-6 secretion by cells that were incubated with HD serum suggests a potential effect of uremia in the intestinal inflammatory response.

scholarly journals Intestinal cyto differentiation in vitro of chick stomach endoderm induced by the duodenal mesenchyme

Development ◽  
1984 ◽  
Vol 82 (1) ◽  
pp. 163-176
Author(s):  
Atsuko Ishizuya-Oka ◽  
Takeo Mizuno
Keyword(s):  
Electron Microscopy ◽  
Epithelial Cells ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cells ◽  
Goblet Cells ◽  
Secretory Cells ◽  
Chick Embryos ◽  
Intestinal Epithelial ◽  
Self Differentiation

The inductive action of duodenal mesenchyme on the cytodifferentiation of stomach endoderm in chick embryos was investigated in vitro with electron microscopy and immunofluorescence. Morphologically undifferentiated endoderm of the stomach of a 4-day embryo could differentiate only into a mucous secretory epithelium when cultured in the absence of mesenchyme. However, when cultivated in recombination with 6-day duodenal mesenchyme, most cells of 4-day stomach endoderm differentiated into intestinal absorptive cells possessing striated border and sucrase, and goblet cells, but not into stomach-type mucous secretory cells. In contrast, when 4-day stomach endoderm was cultured recombined with mesenchyme of embryonic digestive organs other than intestine, none of the stomach endoderm cells differentiated into intestinal epithelial cells. The competence of stomach endoderm for intestinal cytodifferentiation decreased rapidly with development, but remained until relatively later stages in the gizzard region. The present investigation demonstrates that duodenal mesenchyme can induce stomach endoderm, which has acquired the potency for self-differentiation into stomach-type epithelium, to cytodifferentiate into intestinal epithelium.

scholarly journals Protective Effects of Lactoferrin against SARS-CoV-2 Infection In Vitro

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 328 ◽  
Author(s):  
Claudio Salaris ◽  
Melania Scarpa ◽  
Marina Elli ◽  
Alice Bertolini ◽  
Simone Guglielmetti ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Plaque Assay ◽  
Immune Response Gene ◽  
Intestinal Epithelial ◽  
Antiviral Immune Response ◽  
Qrt Pcr ◽  
Anti Inflammatory

SARS-CoV-2 is a newly emerging virus that currently lacks curative treatments. Lactoferrin (LF) is a naturally occurring non-toxic glycoprotein with broad-spectrum antiviral, immunomodulatory and anti-inflammatory effects. In this study, we assessed the potential of LF in the prevention of SARS-CoV-2 infection in vitro. Antiviral immune response gene expression was analyzed by qRT-PCR in uninfected Caco-2 intestinal epithelial cells treated with LF. An infection assay for SARS-CoV-2 was performed in Caco-2 cells treated or not with LF. SARS-CoV-2 titer was determined by qRT-PCR, plaque assay and immunostaining. Inflammatory and anti-inflammatory cytokine production was determined by qRT-PCR. LF significantly induced the expression of IFNA1, IFNB1, TLR3, TLR7, IRF3, IRF7 and MAVS genes. Furthermore, LF partially inhibited SARS-CoV-2 infection and replication in Caco-2 intestinal epithelial cells. Our in vitro data support LF as an immune modulator of the antiviral immune response with moderate effects against SARS-CoV-2 infection.

The effect of berberine in vitro on tight junctions in human Caco-2 intestinal epithelial cells

Fitoterapia ◽  
2009 ◽  
Vol 80 (4) ◽  
pp. 241-248 ◽  
Author(s):  
Lili Gu ◽  
Ning Li ◽  
Qiurong Li ◽  
Qiang Zhang ◽  
Chengyang Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial
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