Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Høgåsen, A.K. et al.

There is no difference in spontaneous and 17 beta-estradiol-induced interleukin-1 beta release by peripheral blood mononuclear cells from nonosteoporotic women with different rates of early postmenopausal bone loss.

Interleukin-1 ( IL-1) is a potent stimulator of bone resorption, and a causal role for IL-1 has been suggested in postmenopausal bone loss. We have examined IL-1 beta release in vitro by peripheral blood mononuclear cells (PBMC) isolated from nonosteoporotic women 9-15 yr after menopause. These women had presented 6 yr previously with significant differences in the rate of early postmenopausal bone loss. Ten women with low rates of bone loss (median 2.0% per year) and 10 women with high rates of bone loss (median 4.9% per year) were included in the study. The women with a high rate of bone loss had a significantly lower bone mass of the lumbar vertebrae compared with that of the other group, but there were no differences in biochemical markers of bone metabolism between the groups (pyridinoline/creatinine ratio in urine and collagen 1 c-terminal telopeptide and bone gla protein in serum). Moreover, there was no difference in spontaneous IL-1 beta release by PBMCs between the two groups and no correlation between IL-1 beta release and present bone turnover, as judged by biochemical markers. Treatment of PBMCs with 10 nmol/L 17 beta-estradiol in vitro significantly stimulated IL-1 beta production in both groups. We conclude that IL-1 beta production by PBMCs in vitro does not correlate with the rate of early postmenopausal bone loss.[1]

References

There is no difference in spontaneous and 17 beta-estradiol-induced interleukin-1 beta release by peripheral blood mononuclear cells from nonosteoporotic women with different rates of early postmenopausal bone loss. Høgåsen, A.K., Nordsletten, L., Aasen, A.O., Falch, J.A. J. Clin. Endocrinol. Metab. (1995) [Pubmed]

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