scholarly journals Interferon-gamma directly affects barrier function of cultured intestinal epithelial monolayers.

1989 ◽  
Vol 83 (2) ◽  
pp. 724-727 ◽  
Author(s):  
J L Madara ◽  
J Stafford
Keyword(s):  
Interferon Gamma ◽  
Barrier Function ◽  
Intestinal Epithelial ◽  
Epithelial Monolayers

The role of caspase-3 in lipopolysaccharide-mediated disruption of intestinal epithelial tight junctions

2006 ◽  
Vol 84 (10) ◽  
pp. 1043-1050 ◽  
Author(s):  
Alex C. Chin ◽  
Andrew N. Flynn ◽  
Jason P. Fedwick ◽  
Andre G. Buret
Keyword(s):  
Escherichia Coli ◽  
Tight Junctions ◽  
Intestinal Permeability ◽  
Barrier Function ◽  
Caspase 3 ◽  
Parp Cleavage ◽  
Intestinal Epithelial ◽  
Epithelial Permeability ◽  
Epithelial Monolayers

The mechanisms responsible for microbially induced epithelial apoptosis and increased intestinal permeability remain unclear. This study assessed whether purified bacterial lipopolysaccharide (LPS) increases epithelial apoptosis and permeability and whether these changes are dependent on caspase-3 activation. In nontumorigenic epithelial monolayers, Escherichia coli O26:B6 LPS increased apoptosis, as shown by nuclear breakdown, caspase-3 activation, and PARP cleavage, and induced disruption of tight junctional ZO-1. Apical, but not basolateral, exposure to LPS increased epithelial permeability. Addition of a caspase-3 inhibitor abolished the effects of LPS. The findings describe a novel mechanism whereby apical LPS may disrupt epithelial tight junctional ZO-1 and barrier function in a caspase-3-dependent fashion.

scholarly journals Transforming Growth Factor β1 Ameliorates Intestinal Epithelial Barrier Disruption by Cryptosporidium parvum In Vitro in the Absence of Mucosal T Lymphocytes

2000 ◽  
Vol 68 (10) ◽  
pp. 5635-5644 ◽  
Author(s):  
James K. Roche ◽  
Clovis A. P. Martins ◽  
Rosana Cosme ◽  
Ronald Fayer ◽  
Richard L. Guerrant
Keyword(s):  
Epithelial Cell ◽  
Barrier Function ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Epithelial Barrier Function ◽  
Epithelial Monolayers ◽  
Tgf Β1

ABSTRACT Exposure to oocysts of the protozoan Cryptosporidium parvum causes intestinal epithelial cell dysfunction in vivo and in vitro, but effective means by which mucosal injury might be prevented remain unclear. We examined the ability of transforming growth factor β1 (TGF-β1)—a cytokine synthesized and released by cells in the intestine—to preserve the barrier function of human colonic epithelia when challenged with C. parvum oocysts and then studied the mechanisms involved. Epithelial barrier function was monitored electrophysiologically, receptors for TGF-β1 were localized by confocal microscopy, and TGF-β1-induced protein kinase C activation was detected intracellularly by translocation of its α isozyme. TGF-β1 alone enhanced intestinal epithelial barrier function, while exposure to C. parvum oocysts (≥105/monolayer) markedly reduced barrier function to ≤40% of that of the control. When epithelial monolayers were pretreated with TGF-β1 at 5.0 ng/ml, the barrier-disrupting effect ofC. parvum oocysts was almost completely abrogated for 96 h. Further investigation showed that (i) the RI and RII receptors for TGF-β1 were present on 55 and 65% of human epithelial cell line cells, respectively, over a 1-log-unit range of receptor protein expression, as shown by flow cytometry and confirmed by confocal microscopy; (ii) only basolateral and not apical TGF-β1 exposure of the polarized epithelial monolayer resulted in a protective effect; and (iii) TGF-β1 had no direct effect on the organism in reducing its tissue-disruptive effects. In exploring mechanisms to account for the barrier-preserving effects of TGF-β1 on epithelium, we found that the protein kinase C pathway was activated, as shown by translocation of its 80-kDa α isozyme within 30 s of epithelial exposure to TGF-β1; the permeability of epithelial monolayers to passage of macromolecules was reduced by 42% with TGF-β1, even in the face of active protozoal infection; and epithelial cell necrosis monitored by lactate dehydrogenase release was decreased by 50% 70 h after oocyst exposure. Changes in epithelial function, initiated through an established set of surface receptors, likely accounts for the remarkable barrier-sparing effect of nanogram-per-milliliter concentrations of TGF-β1 when human colonic epithelium is exposed to an important human pathogen, C. parvum.

scholarly journals Self-organized intestinal epithelial monolayers in crypt and villus-like domains show effective barrier function

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Gizem Altay ◽  
Enara Larrañaga ◽  
Sébastien Tosi ◽  
Francisco M. Barriga ◽  
Eduard Batlle ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Epithelial ◽  
Epithelial Monolayers ◽  
Effective Barrier ◽  
Self Organized

Nitric oxide mediates interferon-gamma-induced hyperpermeability in cultured human intestinal epithelial monolayers

1995 ◽  
Vol 23 (7) ◽  
pp. 1170-1176 ◽  
Author(s):  
Naoki Unno ◽  
Michael J. Menconi ◽  
Marianne Smith ◽  
Mitchell P. Fink
Keyword(s):  
Nitric Oxide ◽  
Interferon Gamma ◽  
Intestinal Epithelial ◽  
Epithelial Monolayers

scholarly journals Author Correction: Self-organized intestinal epithelial monolayers in crypt and villus-like domains show effective barrier function

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Gizem Altay ◽  
Enara Larrañaga ◽  
Sébastien Tosi ◽  
Francisco M. Barriga ◽  
Eduard Batlle ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Epithelial ◽  
Epithelial Monolayers ◽  
Effective Barrier ◽  
Self Organized

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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