Relationship between 17-ß-estradiol and prolactin in the regulation of natural killer cell activity during progression of endometriosis

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Advanced endometriosis stages correlate with increased estradiol, decreased prolactin, and impaired NK cell cytotoxicity, while early stages show hormonal changes without NK activity alteration.

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This study evaluated correlations among plasma 17-β-estradiol (E2), prolactin (PRL), and other neurohormones with natural killer (NK) cell cytotoxic activity and NK cell numbers across women at different stages of endometriosis (early stages I/II vs advanced stages III/IV), comparing findings to healthy subjects. Early-stage patients showed increased E2 or PRL without significant changes in NK activity, whereas advanced stages showed further increased E2, decreased PRL (with an increased E2/PRL ratio), and impaired NK cytotoxicity; NK cytotoxicity in advanced stages correlated with E2, PRL, and the E2/PRL ratio. The peripheral CD16+ or CD56+ NK cell counts/percentages were not significantly different across groups, and progesterone and luteinizing hormone were not significantly changed, while follicle-stimulating hormone decreases were not correlated with NK activity; a stated caveat is that additional studies are needed to determine whether the E2/PRL ratio could serve as a biochemical marker. This paper is centrally about endometriosis — it links the E2/PRL balance to regulation of NK cell activity during disease progression.

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Abstract

Endometriosis is an estrogen-dependent disease affecting women during their reproductive years. An abnormal immune function and, in particular, a decreased natural killer (NK) cell activity have been found in endometriosis, suggesting a role of the immune system in the pathophysiology of the disease. We have recently evidenced a significant inverse relationship between 17-beta-estradiol plasma levels and NK cytotoxicity in endometriosis patients. In this study we have investigated the combined role of 17-beta-estradiol (E2) and prolactin (PRL) in the regulation of NK cell activity during the progression of endometriosis, by evaluating the correlation among E2, PRL, and other immunomodulating neurohormones on both the cytotoxic activity and the number of NK cells in women at different stages of endometriosis. The early stages (I/II) of endometriosis are characterized by increased plasma levels of either E2 or PRL without significant alterations of NK cell activity in comparison with healthy subjects. The progression to advanced stages (III/IV) of the disease is associated with a further increase of E2 levels, a decrease of PRL plasma concentrations (with an increase of E2/PRL ratio), and an impairment of NK cytotoxicity. The plasma levels of both E2 and PRL and the E2/PRL ratio are significantly correlated with the values of NK cytotoxicity in advanced stages of endometriosis. Either the absolute number or the relative percentage of CD16+ or CD56+ peripheral lymphocytes are not significantly different between patients at either stages I/II or III/IV and healthy controls. Plasma levels of progesterone (P) and luteinizing hormone (LH), are not significantly changed in different stages of endometriosis with respect to healthy controls. The significant decrease of follicle-stimulating hormone (FSH) plasma levels found in either stages I/II or III/IV endometriosis patients is not correlated with the NK cell activity. In conclusion, at advanced stages of endometriosis the impairment of NK cell activity occurs with increased E2, and decreased PRL plasma levels. Additional studies are required to determine whether the E2/PRL ratio represents a possible biochemical marker of endometriosis.
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Abstract

Endometriosis is an estrogen-dependent disease affecting women during their reproductive years. An abnormal immune function and, in particular, a decreased natural killer (NK) cell activity have been found in endometriosis, suggesting a role of the immune system in the pathophysiology of the disease. We have recently evidenced a significant inverse relationship between 17-ß-estradiol plasma levels and NK cytotoxicity in endometriosis patients. In this study we have investigated the combined role of 17-ß-estradiol (E2) and prolactin (PRL) in the regulation of NK cell activity during the progression of endometriosis, by evaluating the correlation among E2, PRL., and other immunomodulating neurohormones on both the cytotoxic activity and the number of NK cells in women at different stages of endometriosis. The early stages (I/II) of endometriosis are characterized by increased plasma levels of either E2 or PRL without significant alterations of NK cell activity in comparison with healthy subjects. The progression to advanced stages (III/IV) of the disease is associated with a further increase of E2 levels, a decrease of PRL plasma concentrations (with an increase of E2/PRL ratio), and an impairment of NK cytotoxicity. The plasma levels of both E2 and PRL and the E2/PRL ratio are significantly correlated with the values of NK cytotoxicity in advanced stages of endometriosis. Either the absolute number or the relative percentage of CD16+ or CD56+ peripheral lymphocytes are not significantly different between patients at either stages I/II or III/IV and healthy controls. Plasma levels of progesterone (P) and luteinizing hormone (LH), are not significantly changed in different stages of endometriosis with respect to healthy controls. The significant decrease of follicle-stimulating hormone (FSH) plasma levels found in either stages I/II or III/IV endometriosis patients is not correlated with the NK cell activity. In conclusion, at advanced stages of endometriosis the impairment of NK cell activity occurs with increased E2, and decreased PRL plasma levels. Additional studies are required to determine whether the E2/PRL ratio represents a possible biochemical marker of endometriosis. Similar content being viewed by others

References

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endometriosis

MeSH descriptors

Endometriosis Estradiol Hormones Killer Cells, Natural Prolactin Adult Analysis of Variance Case-Control Studies Cells, Cultured Cytotoxicity, Immunologic Disease Progression Endometriosis Endometriosis Endometriosis Estradiol Female Hormones Humans Killer Cells, Natural Prolactin

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