Estrogen supplements are the primary pharmacologic intervention therapy to prevent and treat loss of bone mass (osteoporosis) in postmenopausal women. Furthermore, at sites of local inflammation near bone, estrogen- deficient women are significantly more susceptible to bone loss than are estrogen-sufficient women. In the present study, we investigate whether estrogen modulates osteoblast (MG-63) production of interleukin-6 (IL-6), an osteoclast recruitment and differentiation of cytokine, in the presence of the proinflammatory cytokine, IL-1β. Using enzyme-linked immunosorbent assay (ELISA), we demonstrate that IL-1β significantly enhances IL-6 secretion into culture supernatants in a dose-dependent and time-dependent manner. Using reverse-transcriptase polymerase chain reaction (RT-PCR) and ELISA respectively, we demonstrate further that levels of 17β-estradiol (active metabolite of estrogen) ≤those found in serum of estrogen-sufficient women inhibit steady-state IL-6 mRNA levels as well as inhibit secretion of IL-6 into culture supernatants. One mechanism by which estrogen therapy preserves bone mass in areas of inflammation may be via inhibition of IL-1β-stimulated obsteoblast-derived IL-6.
ASJC Scopus subject areas
- Cell Biology