scholarly journals The food additive E171 and titanium dioxide nanoparticles indirectly alter the homeostasis of human intestinal epithelial cells in vitro

2019 ◽  
Vol 6 (5) ◽  
pp. 1549-1561 ◽  
Author(s):  
Marie Dorier ◽  
David Béal ◽  
Céline Tisseyre ◽  
Caroline Marie-Desvergne ◽  
Muriel Dubosson ◽  
...  

Repeated exposure to E171 or TiO2-NPs, in vitro, induce moderate inflammation and mucus secretion in intestinal cells.

2016 ◽  
Vol 7 (10) ◽  
pp. 4388-4399 ◽  
Author(s):  
Anouk Kaulmann ◽  
Sébastien Planchon ◽  
Jenny Renaut ◽  
Yves-Jacques Schneider ◽  
Lucien Hoffmann ◽  
...  

Proteomic response of intestinal cells as a model of inflammatory bowel diseases to digested plum and cabbage rich in polyphenols and carotenoids.


2016 ◽  
Vol 79 (11) ◽  
pp. 1965-1970 ◽  
Author(s):  
SANGEETHA ANANDA BASKARAN ◽  
ANUP KOLLANOOR-JOHNY ◽  
MEERA SURENDRAN NAIR ◽  
KUMAR VENKITANARAYANAN

ABSTRACTEscherichia coli O157:H7 is a major foodborne pathogen that can cause serious human illness characterized by hemorrhagic diarrhea and kidney failure. The pathology of enterohemorrhagic E. coli O157:H7 (EHEC) infection is primarily mediated by verotoxins, which bind to the globotriaosylceramide receptor on host cells. Antibiotics are contraindicated for treating EHEC infection because they lead to increased verotoxin release, thereby increasing the risk of renal failure and death in patients. Thus, alternative strategies are needed for controlling EHEC infections in humans. This study investigated the effect of subinhibitory concentrations of five plant-derived antimicrobial agents (PDAs) that are generally considered as safe, i.e., trans-cinnamaldehyde, eugenol, carvacrol, thymol, and β-resorcylic acid, on EHEC motility, adhesion to human intestinal epithelial cells, verotoxin production, and virulence gene expression. All tested PDAs reduced EHEC motility and attachment to human intestinal epithelial cells (P < 0.05) and decreased verotoxin synthesis by EHEC. The reverse transcription real-time PCR data revealed that PDAs decreased the expression of critical virulence genes in EHEC (P < 0.05). The results collectively suggest that these PDAs could be used to reduce EHEC virulence, but follow-up studies in animal models are necessary to validate these findings.


Lab on a Chip ◽  
2018 ◽  
Vol 18 (14) ◽  
pp. 2036-2046 ◽  
Author(s):  
Huanhuan Joyce Chen ◽  
Paula Miller ◽  
Michael L. Shuler

A pumpless GI–Liver system using primary human intestinal epithelial cells serves as an improved model for drug studies.


2008 ◽  
Vol 138 (3) ◽  
pp. 469-475 ◽  
Author(s):  
Sumit Bhattacharyya ◽  
Alip Borthakur ◽  
Pradeep K. Dudeja ◽  
Joanne K. Tobacman

2005 ◽  
Vol 45 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Marleen H.M.C. Nuenen ◽  
Rianne A.F. Ligt ◽  
Robert P. Doornbos ◽  
Janneke C.J. Woude ◽  
Ernst J. Kuipers ◽  
...  

2015 ◽  
Vol 89 (8) ◽  
pp. 4311-4318 ◽  
Author(s):  
Jieyan Pan ◽  
Lili Zhang ◽  
Matthew A. Odenwald ◽  
Le Shen ◽  
Jerrold R. Turner ◽  
...  

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.


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