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M200191200v1
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Papers In Press, published online ahead of print April 30, 2002
J. Biol. Chem, 10.1074/jbc.M200191200
Submitted on January 8, 2002
Revised on April 8, 2002
Accepted on April 29, 2002

Novel mode of interference with NF-AT regulation in T-cells by the bacterial metabolite n-butyrate

Christos Diakos, Eva E. Prieschl, Marcus D. Säemann, Veronica Novotny, Georg A. Böhmig, Robert Csonga, Thomas Baumruker, and Gerhard J. Zlabinger

Institute of Immunology, Vienna A-1090

Corresponding Author: gerhard.zlabinger{at}univie.ac.at

The transcription factor NF-AT plays an essential role in the activation of many early immune response genes. A dynamic equilibrium between calcineurin and cellular kinases controls its phosphorylation and thus regulates its activity by determining its subcellular localization. Here, we demonstrate that T-cell activation in the presence of the bacterial metabolite n-butyrate which leads to inhibition of IL-2 transcription is characterized by the maintenance of the activity of counter-regulatory kinases glycogen synthase kinase 3 and protein kinase A as well as persistence of intracellular cAMP levels, while calcium response and mitogen-activated protein kinase activation were indistinguishable from cells stimulated in the absence of n-butyrate. Nuclear binding of NF-AT was decreased but other transcription factors implicated in IL-2 expression such as AP1 and NFkB were unaffected. The effect on NF-AT binding appeared to be due to increased nuclear export since the export inhibitor leptomycin B completely restored nuclear binding of NF-AT. We, therefore, provide first evidence for interference with NF-AT regulation alternative to the currently understood inhibition of nuclear import. This mechanism might represent a bacterial strategy to subvert host defense which could be of particular clinical importance in the gastrointestinal tract where high amounts of n-butyrate are physiologically present.


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