scholarly journals 692 – Escherichia Coli Heat-Stable Toxin Impairs Colonic Epithelial Barrier Function Via Cgmp-Induced Oxidative Stress, Apoptosis, and Nf-ΚB Activation

2019 ◽  
Vol 156 (6) ◽  
pp. S-151
Author(s):  
Ting Zheng ◽  
Shi-Yi Zhou ◽  
Sha Huang ◽  
Jason Spence ◽  
Chung Owyang
Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2271 ◽  
Author(s):  
Massimiliano G. Bianchi ◽  
Martina Chiu ◽  
Giuseppe Taurino ◽  
Furio Brighenti ◽  
Daniele Del Rio ◽  
...  

The possibility of counteracting inflammation-related barrier defects with dietary compounds such as (poly)phenols has raised much interest, but information is still scarce. We have investigated here if (+)-catechin (CAT) and procyanidin B2 (PB2), two main dietary polyphenols, protect the barrier function of intestinal cells undergoing inflammatory stress. The cell model adopted consisted of co-cultured Caco-2 and HT29-MTX cells, while inflammatory conditions were mimicked through the incubation of epithelial cells with the conditioned medium of activated macrophages (MCM). The epithelial barrier function was monitored through trans-epithelial electrical resistance (TEER), and ROS production was assessed with dichlorofluorescein, while the expression of tight-junctional proteins and signal transduction pathways were evaluated with Western blot. The results indicated that MCM produced significant oxidative stress, the activation of NF-κB and MAPK pathways, a decrease in occludin and ZO-1 expression, and an increase in claudin-7 (CL-7) expression, while TEER was markedly lowered. Neither CAT nor PB2 prevented oxidative stress, transduction pathways activation, ZO-1 suppression, or TEER decrease. However, PB2 prevented the decrease in occludin expression and both polyphenols produced a huge increase in CL-7 abundance. It is concluded that, under the conditions adopted, CAT and PB2 do not prevent inflammation-dependent impairment of the epithelial barrier function of intestinal cell monolayers. However, the two compounds modify the expression of tight-junctional proteins and, in particular, markedly increase the expression of CL-7. These insights add to a better understanding of the potential biological activity of these major dietary flavan-3-ols at intestinal level.


2016 ◽  
Vol 101 (7) ◽  
pp. 801-810 ◽  
Author(s):  
Fan Liu ◽  
Jeremy J. Cottrell ◽  
John B. Furness ◽  
Leni R. Rivera ◽  
Fletcher W. Kelly ◽  
...  

Author(s):  
Adam Comstock ◽  
Asamanja Chattoraj ◽  
Shyamala Ganesan ◽  
Sangbrita Chattoraj ◽  
Marc B. Hershenson ◽  
...  

2013 ◽  
Vol 81 (8) ◽  
pp. 2819-2827 ◽  
Author(s):  
Clément Ngendahayo Mukiza ◽  
J. Daniel Dubreuil

ABSTRACTEscherichia coliheat-stable toxin b (STb) causes diarrhea in animals. STb binds to sulfatide, its receptor, and is then internalized. In the cytoplasm, through a cascade of events, STb triggers the opening of ion channels, allowing ion secretion and water loss and leading to diarrhea. Tight junctions (TJs) are well known for controlling paracellular traffic of ions and water by forming a physical intercellular barrier in epithelial cells, and some bacterial toxins are known to affect adversely TJs. The present study aimed at determining the effect of STb on TJs. T84 cells were treated for 24 h with purified STb and a nontoxic STb mutant (D30V). Transepithelial resistance (TER), paracellular flux marker, and confocal microscopy were used to analyze the effect of STb on TJs. Purified STb caused a significant reduction of TER parallel to an increase in paracellular permeability compared to the results seen in untreated cells or mutant D30V. The increased paracellular permeability was associated with a marked alteration of F-actin stress fibers. F-actin filament dissolution and condensation were accompanied by redistribution and/or fragmentation of ZO-1, claudin-1, and occludin. These changes were also observed following treatment of T84 cells with an 8-amino-acid peptide found in the STb sequence corresponding to a consensus sequence ofVibrio choleraeZot toxin. These effects were not observed with a scrambled peptide or mutant D30V. Our findings indicate that STb induces epithelial barrier dysfunction through changes in TJ proteins that could contribute to diarrhea.


1998 ◽  
Vol 114 ◽  
pp. A904
Author(s):  
R.K. Rao ◽  
R.D. Baker ◽  
S.S. Baker ◽  
C. Wagner ◽  
A. Schluter

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