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Journal of Virology, June 2000, p. 5740-5745, Vol. 74, No. 12
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Prostaglandin E2 Increases Bovine Leukemia Virus tax and pol mRNA Levels via Cyclooxygenase 2: Regulation by Interleukin-2, Interleukin-10, and Bovine Leukemia Virus

Dohun Pyeon,1,dagger Francisco J. Diaz,2 and Gary A. Splitter1,*

Department of Animal Health and Biomedical Sciences1 and Endocrinology-Reproductive Physiology Program,2 University of Wisconsin-Madison, Madison, Wisconsin 53706

Received 29 July 1999/Accepted 29 March 2000

Prostaglandin E2 (PGE2), produced by macrophages, has important immune regulatory functions, suppressing a type 1 immune response and stimulating a type 2 immune response. Type 1 cytokines (interleukin-2 [IL-2], IL-12, and gamma interferon) increase in freshly isolated peripheral blood mononuclear cells (PBMCs) of animals with an early disease stage of bovine leukemia virus (BLV) infection, while IL-10 increases in animals with a late disease stage. Although IL-10 has an immunosuppressive role in the host immune system, IL-10 also inhibits BLV tax and pol mRNA levels in vitro. In contrast, IL-2 stimulates BLV tax and pol mRNA and p24 protein expression in cultured PBMCs. The inhibitory effect of IL-10 on BLV expression depends on soluble factors secreted by macrophages. Thus, we hypothesized that PGE2, a cyclooxygenase 2 (COX-2) product of macrophages, may regulate BLV expression. Here, we show that the level of COX-2 mRNA was decreased in PBMCs treated with IL-10, while IL-2 enhanced the level of COX-2 mRNA. Addition of PGE2 stimulated BLV tax and pol mRNA levels and reversed the IL-10 inhibition of BLV mRNA. In addition, the specific COX-2 inhibitor, NS-398, inhibited the amount of BLV mRNA detected. Addition of PGE2 increased BLV tax mRNA regardless of NS-398 addition. PGE2 inhibited antigen-specific PBMC stimulation, suggesting that stimulation of BLV tax and pol mRNA levels by PGE2 is independent of cell proliferation. These findings suggest that macrophage-derived COX-2 products, such as PGE2, regulate virus expression and disease progression in BLV infection.

* Corresponding author. Mailing address: Department of Animal Health and Biomedical Sciences, University of Wisconsin-Madison, 1656 Linden Dr., Madison, WI 53706. Phone: (608) 262-1837. Fax: (608) 262-7420. E-mail: splitter{at}ahabs.wisc.edu.

dagger Present address: Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115.

Journal of Virology, June 2000, p. 5740-5745, Vol. 74, No. 12
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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