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ToxSci Advance Access published online on February 19, 2004
Toxicological Sciences, doi:10.1093/toxsci/kfh090
Toxicological Sciences © Society of Toxicology 2004; all rights reserved
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Received October 15, 2003; accepted January 24, 2004
© 2004 Society of Toxicology

Immunotoxicology

Altered AP-1 (Activating Protein-1) Activity and c-jun Activation in T Cells Exposed to the Amide Class Herbicide 3,4-Dichloropropionanilide (DCPA)

K. M. Brundage 1, R. Schafer 1, and J. B. Barnett 1*

1 Department of Microbiology, Immunology and Cell Biology, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26506-9177

* To whom correspondence should be addressed. E-mail: jbarnett{at}hsc.wvu.edu.


  Abstract

3,4-dichloropropionanilide (DCPA), the active ingredient of some post-emergence herbicides, has been demonstrated to inhibit several immune system functions including cytokine production by T cells. The central role of cytokines in regulating the immune response suggests a possible mechanism by which DCPA inhibits the immune system. Since interleukin (IL)-2 is critical in regulating many immune functions, we chose to investigate the effect of DCPA on this cytokine. Using the human T lymphoma line, Jurkat, stimulated with phorbol-12-myristate acetate (PMA) and the calcium ionophore A23187 (Io), we determined that DCPA exposure decreased IL-2 secretion and mRNA levels in a dose dependent manner. We hypothesized that DCPA affected one or more of the transcription factors that regulate IL-2 gene transcription. AP-1 is a transcription factor that has been demonstrated to be required for optimal IL-2 gene transcription. Electrophoretic mobility shift assays (EMSAs) demonstrated a decreased level of AP-1 DNA binding activity in DCPA-exposed Jurkat cells compared to control cells from 30 min to 2 h after stimulation. The altered AP-1 DNA binding kinetics was associated with a decrease in c-jun protein in these cells at 1 and 2 h after exposure and a decreased level of phosphorylated c-jun at 1-4 h after exposure. These results suggest a possible mechanism for DCPA induced IL-2 inhibition; alteration in the activation of the c-jun component of AP-1.

Key Words: 3,4-dichloropropionanilide, AP-1, c-jun, IL-2, T cell, propanil .


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T. L. Lewis, K. M. Brundage, R. A. Brundage, and J. B. Barnett
3,4-Dichloropropionanilide (DCPA) Inhibits T-Cell Activation by Altering the Intracellular Calcium Concentration following Store Depletion
Toxicol. Sci., May 1, 2008; 103(1): 97 - 107.
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