scholarly journals The early life microbiota protects neonatal mice from pathological small intestinal epithelial cell shedding

2020 ◽  
Vol 34 (5) ◽  
pp. 7075-7088 ◽  
Author(s):  
Kevin R. Hughes ◽  
Zoe Schofield ◽  
Matthew J. Dalby ◽  
Shabhonam Caim ◽  
Lisa Chalklen ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Early Life ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Neonatal Mice ◽  
Small Intestinal Epithelial Cell ◽  
Small Intestinal ◽  
Cell Shedding

scholarly journals The early life microbiota protects neonatal mice from pathological small intestinal epithelial cell shedding

2019 ◽  
Author(s):  
Kevin R Hughes ◽  
Z Schofield ◽  
MJ Dalby ◽  
S Caim ◽  
L Chalklen ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Gut Microbiota ◽  
Early Life ◽  
Intestinal Epithelial Cell ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Neonatal Mice ◽  
Small Intestinal ◽  
The Impact ◽  
Cell Shedding

AbstractThe gut microbiota plays a crucial role in regulating and maintaining the epithelial barrier, particularly during early life. Notably, patients with chronic intestinal inflammation have a dysregulated process of renewal and replenishment of the intestinal epithelial cell (IEC) barrier, which is linked to disturbances in the gut microbiota. To date, there are no studies focussed on understanding the impact of inflammatory cell shedding events during the early life developmental window, and which host and microbial factors mediate these responses. Here we sought to determine pathological cell shedding outcomes throughout the postnatal developmental period (day 14, 21, 29 and week 8). Surprisingly neonatal mice (day 14 and 21) were highly refractory to induction of cell shedding after intraperitoneal administration of LPS, with day 29 mice showing strong pathological responses, more similar to those observed in adult mice. These differential responses were not linked to defects in the cellular mechanisms and pathways known to regulate cell shedding responses, although we did observe that neonatal mice had elevated anti-inflammatory (IL-10) responses. Notably, when we profiled microbiota and metabolites from these mice, we observed significant alterations. Neonatal mice had high relative abundances of Streptococcus, Escherichia and Enterococcus and increased primary bile acids. In contrast, older mice were dominated by Candidatus Arthromitus, Alistipes and Lachnoclostridium, and had increased concentrations of SCFAs and methyamines. Faecal microbiota transplant (FMT) and antibiotic studies confirmed the importance of early life gut microbiota in cell shedding responses. In these studies, neonates treated with antibiotics restored LPS-induced small intestinal cell shedding, whereas adult FMT alone had no effect. Our findings further support the importance of the early life window for microbiota-epithelial interactions in the presence of inflammatory stimuli and highlight areas for further investigation to probe underlying mechanisms to drive therapeutic development within the context of chronic inflammatory intestinal diseases.

Lipid Composition of Liposomal Membrane Largely Affects Its Transport and Uptake through Small Intestinal Epithelial Cell Models

Lipids ◽  
2020 ◽  
Vol 55 (6) ◽  
pp. 671-682 ◽  
Author(s):  
Keisuke Konishi ◽  
Lei Du ◽  
Grégory Francius ◽  
Michel Linder ◽  
Tomoaki Sugawara ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Lipid Composition ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
Liposomal Membrane ◽  
Small Intestinal Epithelial Cell ◽  
Small Intestinal

Oxygen free radical injury of IEC-18 small intestinal epithelial cell monolayers

1991 ◽  
Vol 100 (6) ◽  
pp. 1533-1543 ◽  
Author(s):  
Thomas Y. Ma ◽  
Daniel Hollander ◽  
Doug Freeman ◽  
Thang Nguyen ◽  
Pavel Krugliak
Keyword(s):  
Free Radical ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Oxygen Free Radical ◽  
Intestinal Epithelial ◽  
Cell Monolayers ◽  
Small Intestinal Epithelial Cell ◽  
Epithelial Cell Monolayers ◽  
Small Intestinal

scholarly journals Transport and uptake effects of marine complex lipid liposomes in small intestinal epithelial cell models

2016 ◽  
Vol 7 (4) ◽  
pp. 1904-1914 ◽  
Author(s):  
Lei Du ◽  
Yu-Hong Yang ◽  
Jie Xu ◽  
Yu-Ming Wang ◽  
Chang-Hu Xue ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Monolayer ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
M Cell ◽  
Small Intestinal Epithelial Cell ◽  
Complex Lipid ◽  
Small Intestinal ◽  
Lipid Liposomes

Transport and uptake effects of marine complex lipid liposomes in Caco-2 and M cell monolayer models.

scholarly journals Toxoplasma gondii Induces Apoptosis via Endoplasmic Reticulum Stress-Derived Mitochondrial Pathway in Human Small Intestinal Epithelial Cell-Line

2021 ◽  
Vol 59 (6) ◽  
pp. 573-583
Author(s):  
Hao Wang ◽  
Chunchao Li ◽  
Wei Ye ◽  
Zhaobin Pan ◽  
Jinhui Sun ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Epithelial Cell ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Host Cell ◽  
Intestinal Epithelial Cell ◽  
Host Cells ◽  
Intestinal Epithelial ◽  
Small Intestinal Epithelial Cell ◽  
Small Intestinal

Toxoplasma gondii, an intracellular protozoan parasite that infects one-third of the world’s population, has been reported to hijack host cell apoptotic machinery and promote either an anti- or proapoptotic program depending on the parasite virulence and load and the host cell type. However, little is known about the regulation of human FHs 74 small intestinal epithelial cell viability in response to T. gondii infection. Here we show that T. gondii RH strain tachyzoite infection or ESP treatment of FHs 74 Int cells induced apoptosis, mitochondrial dysfunction and ER stress in host cells. Pretreatment with 4-PBA inhibited the expression or activation of key molecules involved in ER stress. In addition, both T. gondii and ESP challenge-induced mitochondrial dysfunction and cell death were dramatically suppressed in 4-PBA pretreated cells. Our study indicates that T. gondii infection induced ER stress in FHs 74 Int cells, which induced mitochondrial dysfunction followed by apoptosis. This may constitute a potential molecular mechanism responsible for the foodborne parasitic disease caused by T. gondii.

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