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Emmeline O'Leary1 , Roberto Towns2 , Jennifer Bowen1 *, Daniel Remick3 , P. Landis Keyes1 *
Department of Physiology, University of Michigan Medical School, Ann Arbor, Michigan 1
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 2
Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 3
Macrophages and their cytokine products are present in regressing corpora lutea (CL), yet the actions of cytokines in CL are not clear. We stimulated cytokine production via intraperitoneal injection of 10 µg lipopolysaccharide (LPS) in immature, hypophysectomized rats in which the first set of CL had been induced by exogenous gonadotropins. This model avoids potential compounding effects of cytokines on pituitary gonadotropins. Tail blood was taken 2 h after injection of LPS or saline for assay of tumor necrosis factor a (TNF). Rats were killed 24 or 48 h post-injection and trunk blood was collected for assay of 20a-dihydroprogesterone (DHP), the major luteal steroid in hypophysectomized rats. Ovaries were processed for immunohistochemistry. TNF was elevated (p<0.01) in LPS- vs. vehicle-treated rats (88751 ± 26124 vs. 43 ± 14 pg/ml); however, plasma DHP levels were not different. Numbers of luteal monocytes/macrophages were greater (p<0.05) for LPS- vs. vehicle-treated rats at both 24 and 48 h; however, numbers of apoptotic nuclei in CL were not different between treatments at either time point. Other rats were killed 4 h after LPS or saline injection to evaluate earlier responses. Plasma interleukin-6, which responds in this time frame, was elevated in LPS-treated rats. However, again plasma DHP concentration was not different between treatments. Therefore, in hypophysectomized rats, the stimulation of cytokine production by LPS did not impair luteal steroidogenesis, but promoted macrophage recruitment into CL.
This abstract is being presented on Sunday, August 1 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.