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This Article Full Text Full Text (PDF) All Versions of this Article: 294/5/G1268    most recent 00014.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mazzon, E. Articles by Cuzzocrea, S. Search for Related Content PubMed PubMed Citation Articles by Mazzon, E. Articles by Cuzzocrea, S.

INFLAMMATION/IMMUNITY/MEDIATORS

Role of TNF- in ileum tight junction alteration in mouse model of restraint stress

¹Istituto di Ricovero e Cura a Carattere Scientifico Centro Neurolesi "Bonino-Pulejo," Messina; and ²Department of Clinical and Experimental Medicine and Pharmacology, School of Medicine, University of Messina, Messina, Italy

Submitted 9 January 2008 ; accepted in final form 26 February 2008

Restraint stress induces permeability changes in the small intestine, but little is known about the role of tumor necrosis factor (TNF)- in the defects of the TJ function. In the present study, we used tumor necrosis factor-R1 knockout mice (TNF--R1KO) to understand the roles of TNF- on ileum altered permeability function in models of immobilization stress. The genetic TNF- inhibition significantly reduced the degree of 1) TNF- production in ileum tissues; 2) the alteration of zonula occludens-1 (ZO-1), claudin-2, claudin-4, claudin-5, and β-catenin (immunohistochemistry); and 3) apoptosis (TUNEL staining, Bax, Bcl-2 expression). Taken together, our results demonstrate that inhibition of TNF- reduces the tight junction permeability in the ileum tissues associated with immobilization stress, suggesting a possible role of TNF- on ileum barrier dysfunction.

apoptosis; TNF--deficient mice; zonula occludens-1; claudin-2; β-catenin; tight junction

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