scholarly journals Evidence for early presence of intestinal epithelial cell damage in multitrauma patients

Critical Care ◽  
2008 ◽  
Vol 12 (Suppl 2) ◽  
pp. P136
Author(s):  
J De Haan ◽  
J Derikx ◽  
B Relja ◽  
T Lubbers ◽  
MD Luyer ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Intestinal Epithelial

scholarly journals Different Sources of Copper Effect on Intestinal Epithelial Cell: Toxicity, Oxidative Stress, and Metabolism

Metabolites ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 11
Author(s):  
Runxian Li ◽  
Yang Wen ◽  
Gang Lin ◽  
Chengzhen Meng ◽  
Pingli He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Epithelial Cell ◽  
Protein Expression ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Intestinal Epithelial ◽  
Protein Expression Level ◽  
Treatment Groups ◽  
All Treatment

Copper (Cu) is widely used in the swine industry to improve the growth performance of pigs. However, high doses of copper will induce cell damage and toxicity. The aim of this study was to evaluate toxicity, bioavailability, and effects on metabolic processes of varying copper sources using porcine intestinal epithelial cells (IPEC-J2) as a model. The IPEC-J2 were treated with two doses (30 and 120 μM) of CuSO4, Cu Glycine (Cu-Gly), and Cu proteinate (Cu-Pro) for 10 h, respectively. Cell damage and cellular copper metabolism were measured by the changes in cell viability, copper uptake, oxidative stress biomarkers, and gene/protein expression levels. The results showed that cell viability and ratio of reduced and oxidized glutathione (GSH/GSSG) decreased significantly in all treatment groups; intracellular copper content increased significantly in all treatment groups; total superoxide dismutase (SOD) activity increased significantly in the 120 μM exposed groups; SOD1 protein expression levels were significantly upregulated in 30 μM Cu-Pro, 120 μM Cu-Gly, and 120 μM Cu-Pro treatment groups; intracellular reactive oxygen species (ROS) generation and malondialdehyde (MDA) content increased significantly in 30 μM treatment groups and 120 μM CuSO4 treatment group. CTR1 and ATP7A gene expression were significantly downregulated in the 120 μM exposed groups. While upregulation of ATOX1 expression was observed in the presence of 120 μM Cu-Gly and Cu-Pro. ASCT2 gene expression was significantly upregulated after 120 μM Cu-Glycine and CuSO4 exposure, and PepT1 gene expression was significantly upregulated after Cu-Pro exposure. In addition, CTR1 protein expression level decreased after 120 μM CuSO4 and Cu-Gly exposure. PepT1 protein expression level was only upregulated after 120 μM Cu-Pro exposure. These findings indicated that extra copper supplementation can induce intestinal epithelial cell injury, and different forms of copper may have differing effects on cell metabolism.

scholarly journals Total Intermittent Pringle Maneuver during Liver Resection Can Induce Intestinal Epithelial Cell Damage and Endotoxemia

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30539 ◽  
Author(s):  
Simon A. W. G. Dello ◽  
Kostan W. Reisinger ◽  
Ronald M. van Dam ◽  
Marc H. A. Bemelmans ◽  
Toin H. van Kuppevelt ◽  
...  
Keyword(s):  
Liver Resection ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Pringle Maneuver ◽  
Intestinal Epithelial

scholarly journals Gut microbiome–derived metabolites modulate intestinal epithelial cell damage and mitigate graft-versus-host disease

2016 ◽  
Vol 17 (5) ◽  
pp. 505-513 ◽  
Author(s):  
Nathan D Mathewson ◽  
Robert Jenq ◽  
Anna V Mathew ◽  
Mark Koenigsknecht ◽  
Alan Hanash ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Graft Versus Host Disease ◽  
Gut Microbiome ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Intestinal Epithelial ◽  
Host Disease ◽  
Graft Versus Host

scholarly journals Erratum: Corrigendum: Gut microbiome–derived metabolites modulate intestinal epithelial cell damage and mitigate graft-versus-host disease

2016 ◽  
Vol 17 (10) ◽  
pp. 1235-1235 ◽  
Author(s):  
Nathan D Mathewson ◽  
Robert Jenq ◽  
Anna V Mathew ◽  
Mark Koenigsknecht ◽  
Alan Hanash ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Graft Versus Host Disease ◽  
Gut Microbiome ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Intestinal Epithelial ◽  
Host Disease ◽  
Graft Versus Host

Autophagy Deficiency Diminishes Indomethacin-Induced Intestinal Epithelial Cell Damage through Activation of the ERK/Nrf2/HO-1 Pathway

2015 ◽  
Vol 355 (3) ◽  
pp. 353-361 ◽  
Author(s):  
Satoshi Harada ◽  
Takatoshi Nakagawa ◽  
Shunichi Yokoe ◽  
Shoko Edogawa ◽  
Toshihisa Takeuchi ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Intestinal Epithelial

scholarly journals Acid Sphingomyelinase Secretion by Irradiated Endothelial Cells: A Role in Intestinal Epithelial Cell Damage?

2008 ◽  
Vol 43 (5) ◽  
Author(s):  
M.-H. Gaugler ◽  
S. Gouard ◽  
N. Ripoche ◽  
C. Niaudet ◽  
S. Bonnaud ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Acid Sphingomyelinase ◽  
Intestinal Epithelial

scholarly journals Glutamine and Alanyl-Glutamine Increase RhoA Expression and ReduceClostridium difficileToxin-A-Induced Intestinal Epithelial Cell Damage

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Ana A. Q. A. Santos ◽  
Manuel B. Braga-Neto ◽  
Marcelo R. Oliveira ◽  
Rosemeire S. Freire ◽  
Eduardo B. Barros ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Cell Morphology ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Fluorescent Microscopy ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Ki 67

Clostridium difficileis a major cause of antibiotic-associated colitis and is associated with significant morbidity and mortality. Glutamine (Gln) is a major fuel for the intestinal cell population. Alanyl-glutamine (Ala-Gln) is a dipeptide that is highly soluble and well tolerated. IEC-6 cells were used in thein vitroexperiments. Cell morphology was evaluated by atomic force microscopy (AFM) and scanning electron microscopy (SEM). Cell proliferation was assessed by WST-1 and Ki-67 and apoptosis was assessed by TUNEL. Cytoskeleton was evaluated by immunofluorescence for RhoA and F-actin. RhoA was quantified by immunoblotting. TcdA induced cell shrinkage as observed by AFM, SEM, and fluorescent microscopy. Additionally, collapse of the F-actin cytoskeleton was demonstrated by immunofluorescence. TcdA decreased cell volume and area and increased cell height by 79%, 66.2%, and 58.9%, respectively. Following TcdA treatment, Ala-Gln and Gln supplementation, significantly increased RhoA by 65.5% and 89.7%, respectively at 24 h. Ala-Gln supplementation increased cell proliferation by 137.5% at 24 h and decreased cell apoptosis by 61.4% at 24 h following TcdA treatment. In conclusion, TcdA altered intestinal cell morphology and cytoskeleton organization, decreased cell proliferation, and increased cell apoptosis. Ala-Gln and Gln supplementation reduced intestinal epithelial cell damage and increased RhoA expression.

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