17beta-estradiol and progesterone do not influence the production of cytokines from lipopolysaccharide-stimulated monocytes in humans
- PMID: 15474098
- DOI: 10.1016/j.fertnstert.2004.05.072
17beta-estradiol and progesterone do not influence the production of cytokines from lipopolysaccharide-stimulated monocytes in humans
Abstract
Objective: To test whether 17beta-estradiol or progesterone influence the cytokine productive capacity of lipopolysaccharide (LPS)-stimulated monocytes in humans.
Design: Prospective study.
Setting: Academic research institution.
Patient(s): Seven women in the luteal phase of a normal ovarian cycle, 13 oral contraceptive users, 10 men, and 10 postmenopausal women.
Intervention(s): Blood samples collected from women in the luteal phase and from oral contraceptive users were used to study the in vivo effect of 17beta-estradiol and progesterone on monocyte cytokine production. Blood samples collected from men and postmenopausal women were used for in vitro incubation with 17beta-estradiol and progesterone.
Main outcome measure(s): The percentage of monocytes producing tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) after in vitro LPS-stimulation was determined.
Result(s): No in vivo relation in the productive capacities of LPS-stimulated monocytes in the luteal phase of the ovarian cycle was found between progesterone and TNF-alpha or IL-1beta; or between 17beta-estradiol and TNF-alpha or IL-1beta. Moreover, the production of TNF-alpha and IL-1beta by LPS-stimulated monocytes did not vary between periods of oral contraceptive use and nonuse. The production of TNF-alpha and IL-1beta by LPS-stimulated monocytes in the blood of men and postmenopausal women in vitro was not influenced by incubation with different concentrations of 17beta-estradiol or progesterone.
Conclusion(s): We could not find evidence for a causal relationship between 17beta-estradiol or progesterone and TNF-alpha- or IL-1beta-production. We conclude that 17beta-estradiol and progesterone do not influence the cytokine-production capacity of LPS-stimulated monocytes in humans.
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