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Journal of Virology, August 2007, p. 8406-8411, Vol. 81, No. 16
0022-538X/07/$08.00+0     doi:10.1128/JVI.00155-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Expression of the Mu Opioid Receptor in the Human Immunodeficiency Virus Type 1 Transgenic Rat Model{triangledown}

Sulie L. Chang,* Jose A. Beltran, and Shilpa Swarup

Department of Biological Sciences, Seton Hall University, 400 South Orange Ave., South Orange, New Jersey 07079

Received 23 January 2007/ Accepted 24 May 2007

Opioids, via the mu opioid receptor (MOR), can exacerbate bacterial infections and the immunopathogenesis of human immunodeficiency virus type 1 (HIV-1) infection. Recently, an HIV-1 transgenic (HIV-1Tg) rat model containing circulating HIV-1 gp120 was created. Using real-time reverse transcription-PCR, we found that MOR mRNA levels were significantly higher in the peritoneal macrophages of the HIV-1Tg rat than those in control animals. Lipopolysaccharide, a bacterial endotoxin, induced secretion of the inflammatory cytokines tumor necrosis factor alpha (TNF-{alpha}), interleukin-ß (IL-ß), and IL-10 in the HIV-1Tg rat and further increased MOR expression. Ex vivo studies showed that MOR expression was up-regulated in the peritoneal macrophages of F344 control rats by exposure to serum from HIV-1Tg rats and that MOR up-regulation was abolished by addition of gp120 antibody to the serum. In human TPA-differentiated HL-60 cells, which are macrophage-like cells, LPS-induced MOR mRNA up-regulation was greater in gp120-pretreated cells than in vehicle-pretreated cells. Our data suggest that in individuals infected with HIV-1, the MOR is up-regulated, possibly by circulating HIV-1 proteins such as gp120, and HIV-1 proteins may play a significant role in modulating the response to bacterial infection in opioid-using HIV-infected individuals. Furthermore, our results demonstrate that the new HIV-1Tg rat model can be a valuable tool with which to study MOR gene expression and its effects in the continuous presence of HIV viral proteins.

* Corresponding author. Mailing address: Department of Biological Sciences, Seton Hall University, McNulty Hall, Room 322, South Orange, NJ 07079. Phone: (973) 761-9456. Fax: (973) 275-2489. E-mail: changsul{at}shu.edu

{triangledown} Published ahead of print on 6 June 2007.

Journal of Virology, August 2007, p. 8406-8411, Vol. 81, No. 16
0022-538X/07/$08.00+0     doi:10.1128/JVI.00155-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Liu, H., Li, H., Guo, L., Li, C., Li, M., Jiang, W., Liu, X., McNutt, M. A., Li, G. (2009). The mechanism involved in the repression of the {micro} opioid receptor gene expression in CEM x174 cells infected by simian immunodeficiency virus. J. Leukoc. Biol. 85: 684-691 [Abstract] [Full Text]  


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