Tumor Necrosis Factor-α Increases Sodium and Chloride Conductance Across the Tight Junction of CACO-2 BBE, a Human Intestinal Epithelial Cell Line

1998 ◽  
Vol 161 (3) ◽  
pp. 263-274 ◽  
Author(s):  
C.W. Marano ◽  
S.A. Lewis ◽  
L.A. Garulacan ◽  
A. Peralta Soler ◽  
J.M. Mullin
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cell ◽  
Tumor Necrosis ◽  
Intestinal Epithelial Cell ◽  
Tumor Necrosis Factor Α ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cell ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor-α represses the expression of NHE2 through NF-κB activation in intestinal epithelial cell model, C2BBe1

2011 ◽  
Vol 17 (3) ◽  
pp. 720-731 ◽  
Author(s):  
Ruhul Amin ◽  
Temitope Orenuga ◽  
Sangeeta Tyagi ◽  
Pradeep K. Dudeja ◽  
Krishnamurthy Ramaswamy ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cell ◽  
Tumor Necrosis ◽  
Intestinal Epithelial Cell ◽  
Tumor Necrosis Factor Α ◽  
Cell Model ◽  
Intestinal Epithelial ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Activation of muscarinic cholinoceptor ameliorates tumor necrosis factor-α-induced barrier dysfunction in intestinal epithelial cells

FEBS Letters ◽  
2015 ◽  
Vol 589 (23) ◽  
pp. 3640-3647 ◽  
Author(s):  
Md Rafiqul Islam Khan ◽  
Junsuke Uwada ◽  
Takashi Yazawa ◽  
Md Tariqul Islam ◽  
Susanne M. Krug ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Factor Α ◽  
Necrosis Factor

Monocyte/macrophages evoke epithelial dysfunction: indirect role of tumor necrosis factor-α

1998 ◽  
Vol 275 (4) ◽  
pp. C932-C939 ◽  
Author(s):  
Mehri Zareie ◽  
Derek M. McKay ◽  
Garrett G. Kovarik ◽  
Mary H. Perdue
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Epithelial Cell Line ◽  
Ussing Chambers ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

We examined the ability of monocytes (MΦ) activated by bacterial products to alter epithelial physiology. Confluent monolayers of the T84 colonic epithelial cell line were grown on filter supports and then cocultured in the presence of human MΦ with or without the activating agents bacterial lipopolysaccharide and the bacterial tripeptide formyl-methionyl-leucyl-phenylalanine. After 24 or 48 h, monolayers were mounted in Ussing chambers where parameters of epithelial function were measured. Exposure to activated MΦ resulted in a significant increase ( P < 0.05) in baseline short-circuit current (250% after 48 h) that was associated with enhanced secretion of Cl−. In addition, epithelial permeability was significantly increased as shown by reduced transepithelial resistance and increased flux of51Cr-EDTA. Activated MΦ produced substantial amounts (∼3 ng/ml at 48 h) of tumor necrosis factor-α (TNF-α). TNF-α was identified as a key mediator acting via an autocrine mechanism to induce epithelial pathophysiology. Our data show that MΦ, when activated by common bacterial components, are potent effector cells capable of initiating significant changes in the transport and barrier properties of a model epithelium.

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