Hormonal modulation of interleukin-6, tumor necrosis factor and associated receptor secretion in postmenopausal women

Esther M. Brooks-Asplund, Carrie E. Tupper, Jane M. Daun, W. Larry Kenney, Joseph G. Cannon

Research output: Contribution to journalArticlepeer-review

46 Scopus citations


Hormone replacement therapy (HRT) reduces the risk for osteoporosis but transiently increases cardiovascular risk for some postmenopausal women. This study investigated the hypothesis that these risks are associated with HRT-induced changes in mononuclear cell secretion of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and associated soluble receptors. Compared to the untreated condition (n=8), estrogen therapy (n=7) and estrogen+progestin therapy (n=7) both caused 2-fold elevations in TNF-α secretion. IL-6 secretion was increased (48%, P=0.04) only by estrogen+progestin therapy. Although soluble receptor secretion was not different among groups, soluble TNF receptor type I and IL-6 receptor secretion were inversely related to plasma follicle stimulating hormone (P<0.05). Both therapies reduced plasma osteocalcin (a marker for osteoporosis) by ∼50% (P<0.002). Plasma C-reactive protein (CRP, a marker for cardiovascular risk) was 3-fold higher in women receiving only estrogen, compared to untreated women (P=0.01), and twice as high as those receiving estrogen+progestin (P=0.045). Simple linear relationships were not observed between cytokine secretion and these markers, but a significant HRT/TNF-α interaction with osteocalcin (P=0.022) and an HRT/IL-6 interaction with CRP (P=0.016) indicated more complex relationships between hormone replacement, cytokine activity, and health risks associated with menopause.

Original languageEnglish (US)
Pages (from-to)193-200
Number of pages8
Issue number4
StatePublished - 2002
Externally publishedYes


  • Bone turnover
  • C-reactive protein
  • Estrogen
  • FSH
  • Progestin

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology


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