Aflatoxin B1 modulates the expression of phenotypic markers and cytokines by splenic lymphocytes of male F344 rats. Issue 3 (19th March 2013)

• Record Type: Journal Article
• Authors: Qian, Guoqing; Tang, Lili; Guo, Xia; Wang, Franklin; Massey, Michael E.; Su, Jianjia; Guo, Tai L.; Williams, Jonathan H.; Phillips, Timothy D.; Wang, Jia‐Sheng
• Is Part Of: Journal of applied toxicology. Volume 34:Issue 3(2014)
• Page Start: 241
• Page End: 249
• Publication Date: 2013-03-19
• Subjects: Toxicology -- Periodicals; Industrial toxicology -- Periodicals; Environmentally induced diseases -- Periodicals; Toxicology -- Periodicals; 615.9005
• DOI: 10.1002/jat.2866
• Languages: English
• ISSNs: 0260-437X

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <p>Aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) is immunotoxic to animals and a suspected immunosuppressant in humans. In this study, we investigated the effects of AFB<sub>1</sub> on splenic lymphocyte phenotypes and the inflammatory cytokine expression in male F344 rats. Exposure of animals to AFB<sub>1</sub> [5–75 µg kg<sup>–1</sup> body weight (BW)] for 1 week showed dose‐dependent decreases in the percentage of splenic CD8<sup>+</sup> T cells and CD3<sup>‐</sup>CD8a<sup>+</sup> NK cells. A general inhibition of the expression of interleukin (IL)‐4 and interferon (IFN)‐γ by CD4<sup>+</sup> T cells, IL‐4 and IFN‐γ by CD8a<sup>+</sup> cells, and tumor necrosis factor (TNF)‐α expression by natural killer (NK) cells was also found; however, no concurrent histological changes in spleen tissue were present, suggesting acute immunosuppression without overt toxicity. Five‐week exposure with AFB<sub>1</sub> significantly increased the percentages of CD3<sup>+</sup> and CD8<sup>+</sup> T cells, especially at low doses (≤ 25 µg kg<sup>–1</sup>). AFB<sub>1</sub> treatment significantly decreased the anti‐inflammatory cytokine IL‐4 expression by CD4<sup>+</sup> T cells and significantly increased the pro‐inflammatory cytokine IFN‐γ expression by CD4<sup>+</sup> T cells and TNF‐α expression by NK cells. These results indicated that repeated AFB<sub>1</sub> exposure promotes inflammatory responses by regulating cytokine expression. Our data provides novel insights into the mechanisms by which AFB<sub>1</sub> exposure differentially modulates the cell‐mediated immune responses and suggests the involvement of an inflammatory response upon repeated exposure. Copyright © 2013 John Wiley & Sons, Ltd.</p> </abstract>