Abstract
BackgroundDysregulation of immune response is associated with development of endometriosis. The study aim was to evaluate effect of combined oral contraceptive pills (COCs) consisting of ethinyl estradiol (EE) and desogestrel on the expression of macrophage, natural killer cells, and regulatory T cells of ovarian endometriotic cysts.MethodsEndometriotic cyst wall tissues were collected from women with endometriosis who were treated (n = 22) with COCs (one table per day of EE 0.03 mg and desogestrel 0.15 mg administered for 28 to 35 days before surgery) or untreated (n = 22). The tissues were collected from endometriotic cyst wall during laparoscopic or laparotomy ovarian cystectomy. Immunohistochemistry for anti-CD68, anti-CD56, and anti-forkhead–winged helix transcription factor (FoxP3), a marker for macrophages, natural killer cells, and regulatory T cells, respectively, were investigated.ResultsThe median (interquartile range [IQR]) number of anti-CD68 positive cells in the COC group was significantly lower than in the untreated group (12.7; 4.9–19.3) versus 45.7 (26.0–70.7), p < 0.001). Tissue infiltration of anti-CD56 positive cells in endometriotic cyst was significantly higher after the treatment when compared with tissue from untreated group (42.9, 27.4–68.9 versus 25.3 (14.1–37.3; p = 0.009). The number of regulatory T cells was also significantly increased in the COC group (6.3, 2.8–15.5) versus 0 (0–1.8; p < 0.001).ConclusionsThe effects of COC, containing EE 0.30 mg with desogestrel 0.15 mg, on the immune system was demonstrated by a significant decrease in the number of macrophages and an increase in natural killer and regulatory T cells.
Highlights
Endometriosis is diagnosed when endometrial tissue grows outside the uterus
Women were diagnosed with ovarian endometriotic cysts with sizes equal to or more than 3 cm based on ultrasonography, no previous history of using any oral hormones three months prior to study enrollment, those who did not receive depot-medroxyprogesterone acetate (DMPA) or gonadotropin releasing hormone agonist (GnRH) agonist within nine months prior to study enrollment, and willingness to participate in the study
Tissue infiltration of anti-CD56 positive cells in endometriotic cyst wall tissues was significantly higher in the treatment group compared with the non-treatment group versus 25.3 (14.1–37.3; p = 0.009)
Summary
Endometriosis is diagnosed when endometrial tissue grows outside the uterus. Sampson’s theory, one of many proposed theories, explained that the disease originates from the reversal of blood flow during the menstrual cycle to the pelvic cavity [1]. A dysregulated immune system could cause endometriosis initiation and progression. The retrograde endometrial tissues during menstruation that escape from clearance by the immune response could attach and invade the pelvic cavity structures. The ectopic endometrium stimulates inflammatory responses leading to secretion of various cytokines in tissue, peritoneal fluid. The numerous macrophages in peritoneal fluid of patients with endometriosis secrete many kinds of enhancing cytokines for endometriosis progression, including pro-inflammatory cytokines [7]; tumor growth factor (TGF)-β [8], interleukins (IL)-6 and-10, angiogenic factors, vascular endothelial growth factor (VEGF) [9, 10], and an inhibitory cytokine; IL-24 [11]. Dysregulation of immune response is associated with development of endometriosis. The study aim was to evaluate effect of combined oral contraceptive pills (COCs) consisting of ethinyl estradiol (EE) and desogestrel on the expression of macrophage, natural killer cells, and regulatory T cells of ovarian endometriotic cysts
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