Effect of dehydroepiandrosterone on lipopolysaccharide-induced interleukin-6 production in DH82 cultured canine macrophage cells.
OBJECTIVE: This study examined the effect of dehydroepiandrosterone (DHEA) on lipopolysaccharide (LPS)-stimulated interleukin-6 (IL-6) production in the DH82 canine macrophage cell line. STUDY DESIGN: Cultured DH82 cells were stimulated with varying concentrations of LPS with or without DHEA for various times. Supernatant IL-6 levels were measured by enzyme-linked immunosorbent assay, and cellular cytoplasmic IkappaBalpha protein expression measured by Western blot analysis. RESULTS: LPS dose-dependently stimulated IL-6 production (p=0.016). Cells stimulated with 20 microg LPS showed a time-dependent increase of IL-6 concentration up to 10 h post-treatment (p=0.007). Co-treatment of DH82 cells with 20 microg LPS and various concentrations of DHEA for 14 h showed that up to 10 microM DHEA dose-dependently decreased the IL-6 concentration (p=0.007). Also, addition of 20 microM DHEA to DH82 cells with 20 microg LPS time-dependently decreased the IL-6 concentration for up to 14 h post-treatment (p=0.018). Stimulation of cultured DH82 cells with 20 microg LPS significantly decreased cellular cytoplasmic IkappaBalpha expression, beginning at 30 min post-treatment and persisting to at least 2 h post-treatment (p=0.012). However, co-treatment of cells with 20 microg LPS and 20 microM DHEA abrogated this effect until 2 h post-treatment. CONCLUSIONS: DHEA decreased the IL-6 concentration in the supernatant of LPS-stimulated DH82 cells by inhibiting the sequestration of IkappaBalpha, which is necessary for the activation of nuclear factor-kappa B. These findings provide new insights into the immunomodulatory effects of DHEA.[1]References
- Effect of dehydroepiandrosterone on lipopolysaccharide-induced interleukin-6 production in DH82 cultured canine macrophage cells. Kim, S.K., Shin, M.S., Jung, B.K., Shim, J.Y., Won, H.S., Lee, P.R., Kim, A. J. Reprod. Immunol. (2006) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg