The effects of sex hormones on the in vitro chemotaxis of polymorphonuclear leukocytes (PMNs) and monocytes were investigated using fMLP as the chemoattractant. PMNs, monocytes, and plasma were obtained from heparinized peripheral blood of healthy adults. Chemotaxis of PMNs or monocytes treated with sex hormones were tested using 48-well chemotaxis microchambers. The correlation between sex hormone levels in plasma and the chemotactic ability of PMNs from the same donor was also investigated. The chemotaxis of PMNs was enhanced by progesterone, while it was reduced by estradiol. Random migration of PMNs was also enhanced by progesterone and reduced by estradiol. The effect of estradiol on PMN chemotaxis was inhibited by addition of antiestrogens or progesterone. Testosterone did not have a measurable effect on PMN chemotaxis. A significant positive correlation was found between the concentration of progesterone in plasma of females and PMN chemotactic ability in vitro. For males, there was no significant relationship between plasma levels of sex hormones and PMN chemotactic ability. Estradiol and testosterone levels in plasma did not correlate with PMN chemotactic ability. Sex hormones had no effect on the chemotaxis of monocytes. These results suggest that the altered PMN chemotaxis associated with gingival inflammation may be due to the effects of sex hormones.

The effects of sex hormones on the vitro production of prostaglandin (PG) E2 by monocytes were investigated. Monocytes were obtained from heparinized peripheral blood of healthy adults and incubated for 24 hours with lipopolysaccharide (LPS) and sex hormones. After incubation, the medium was assayed for PGE2 by means of radioimmunoassay. PGE2 production by monocytes was enhanced by progesterone. Estradiol reduced PGE2 production at 0.4 ng/ml, but enhanced it at 20 ng/ml. Testosterone reduced PGE2 production. The reduced PGE2 production by monocytes treated with 0.4 ng/ml of estradiol was restored to the control level by addition of progesterone at 20 ng/ml. These results suggest that sex hormones may modulate gingival inflammation mediated by PGE2.

Estradiol and progesterone inhibited the production of IL-1 from human peripheral monocytes. The inhibition was not the result of enhanced production of PGE2. Under conditions in which sex hormone levels are low, monocytes produce IL- more readily in response to stimulation by LPS than high levels of such hormones. Low concentrations of sex hormones may be considered as one of the risk factors for periodontitis.

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