Differential regulation of interleukins IL-13 and IL-15 by ovarian steroids, TNF-alpha and TGF-beta in human endometrial epithelial and stromal cells

Mol Hum Reprod. 2005 Oct;11(10):751-60. doi: 10.1093/molehr/gah233. Epub 2005 Oct 27.

Abstract

Based on the endometrial spatial and temporal expression of interleukins (ILs) IL-13 and IL-15 during the normal menstrual cycle, we hypothesized that ovarian steroids and non-steroidal factors regulate their expression in a cell-specific manner. To test this hypothesis and determine IL-13/IL-15 actions, we used endometrial epithelial (EEC) and stromal (ESC) cells isolated and cultured under defined conditions. We confirmed the expression of IL-13 and IL-15 in these cells and further demonstrated that 17beta estradiol (E2), medroxyprogesterone acetate (MPA) and their combination differentially regulated their mRNA expression and protein production in a time- and cell-specific manner (P < 0.05). We also showed that tumour necrosis factor-alpha (TNF-alpha; 10 and 25 ng/ml) and transforming growth factor-beta (TGF-beta; 1 and 5 ng/ml), cytokines with inflammatory and immune regulatory functions in a cell- and dose-dependent manner regulate the expression of IL-13 and IL-15 (P < 0.05). Functionally, IL-13 and IL-15 1-100 ng/ml displayed a limited mitogenic activity towards EEC and ESC; however, they regulated the expression of TNF receptor type 1 (TNFR) mRNA and soluble protein in a cell-specific manner (P < 0.05). We conclude that ovarian steroids, TNF-alpha and TGF-beta act as key regulators of endometrial IL-13 and IL-15 expression which act locally regulating TNFR expression in a cell-specific manner. Based on these findings, we conclude that IL-13/IL-15, either alone or through their interactions with other cytokines, influence the outcome of endometrial inflammatory/immune responses during the normal menstrual cycle, and due to their altered expression may extend these processes in dysfunctional bleeding and endometriosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Proliferation
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Endometrium / drug effects
  • Endometrium / metabolism*
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism*
  • Estradiol / pharmacology
  • Female
  • Gene Expression Regulation
  • Gonadal Steroid Hormones / pharmacology*
  • Humans
  • Interleukin-13 / genetics
  • Interleukin-13 / metabolism*
  • Interleukin-15 / genetics
  • Interleukin-15 / metabolism*
  • Medroxyprogesterone Acetate / pharmacology
  • Menstrual Cycle / metabolism
  • Receptors, Tumor Necrosis Factor, Type I / genetics
  • Receptors, Tumor Necrosis Factor, Type I / metabolism
  • Stromal Cells / drug effects
  • Stromal Cells / metabolism
  • Time Factors
  • Transforming Growth Factor beta / pharmacology*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Gonadal Steroid Hormones
  • Interleukin-13
  • Interleukin-15
  • Receptors, Tumor Necrosis Factor, Type I
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Estradiol
  • Medroxyprogesterone Acetate