This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Romano-Carratelli, C. Articles by Metafora, S. Search for Related Content PubMed PubMed Citation Articles by Romano-Carratelli, C. Articles by Metafora, S.

 Previous Article  |  Next Article 

Clinical and Diagnostic Laboratory Immunology, January 2002, p. 115-125, Vol. 9, No. 1
1071-412X/01/$04.00+0     DOI: 10.1128/CDLI.9.1.115-125.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Effect of Protein SV-IV on Experimental Salmonella enterica Serovar Typhimurium Infection in Mice

Institute of Microbiology,¹ Department of Biochemistry and Biophysics,² Department of Experimental Medicine, Medical School, 2nd University of Naples,³ CNR International Institute of Genetics and Biophysics, Naples, Italy⁴

Received 5 July 2001/ Returned for modification 18 September 2001/ Accepted 29 October 2001

Seminal vesicle protein IV (SV-IV) is a secretory anti-inflammatory, procoagulant, and immunomodulatory protein produced in large amounts by the seminal vesicle epithelium of the rat under the strict transcriptional control of androgen. In particular, this protein was shown to possess the ability to markedly inhibit in vivo the humoral and cell-mediated immune responses of mice to nonbacterial cellular antigens (sheep erythrocytes and spermatozoa). We report data that demonstrate that in mice treated with SV-IV and infected with Salmonella enterica serovar Typhimurium, SV-IV is able to downregulate some important immunological and biochemical parameters that serovar Typhimurium normally upregulates in these animals. This event did not correlate with a lower bacterial burden but was associated with a markedly increased one (300%). Furthermore, the treatment of mice with SV-IV alone also produced a significant increase in the rate of mortality among serovar Typhimurium-infected animals. The mechanism underlying these phenomena was investigated, and the strong immunosuppression produced by SV-IV in serovar Typhimurium-infected mice was suggested to be the basis for the increased rate of mortality. The SV-IV-mediated immunosuppression was characterized by a decrease in the humoral and cell-mediated immune responses, altered lymphocyte-macrophage interaction, downregulation of cytokine and inducible nitric oxide synthase gene expression, inhibition of macrophage phagocytosis and intracellular killing activities, and absence of apoptosis in the splenocyte population of SV-IV- and serovar Typhimurium-treated mice. The immunosuppressive activity of SV-IV was specific and was not due to aspecific cytotoxic effects. SV-IV-specific receptors (K_d = 10^-8 M) occurring on the macrophage and lymphocyte plasma membranes may be involved in the molecular mechanism underlying the SV-IV-mediated immunosuppression. Some results obtained by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay also revealed a functional impairment of mitochondria (a decrease in mitochondrial dehydrogenase activity), thus indicating the possible implication of these organelles in the immunosuppressive process.

This article has been cited by other articles:

• Robertson, F. G., Harris, J., Naylor, M. J., Oakes, S. R., Kindblom, J., Dillner, K., Wennbo, H., Tornell, J., Kelly, P. A., Green, J., Ormandy, C. J. (2003). Prostate Development and Carcinogenesis in Prolactin Receptor Knockout Mice. Endocrinology 144: 3196-3205 [Abstract] [Full Text]