Anti-Progesterone polyclonal antibody

Research question: It is not clear whether innate immunity along with autophagy is altered in endometrial cells of patients with endometriosis. Design: This study evaluated the effects of lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C) stimulation on autophagy induction, pro-IL-1 beta expression, and secretion of interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF alpha) in endometrial epithelial and/or stromal cells of patients with endometriosis (EE-endo, ES-endo, respectively), those of patients with hydrosalpinx (EE-hydro, ES-hydro, respectively) and those of healthy fertile women (EE-healthy, ES-healthy, respectively), with and without inhibition of autophagy by autophagy-related (ATG)13 gene small interfering RNA (siRNA). Results: Stimulation with either LPS or poly I:C triggered autophagy in EE/ES-healthy, whereas no significant induction was observed in either EE/ES-endo or EE/ES-hydro. In EE- and/or ES-healthy, IL-1 beta and/or TNF alpha secretion after stimulation with LPS or poly 1:0 was significantly higher in cells with ATG13 knockdown compared with those with siRNA control (P < 0.03), whereas no significant difference was observed in either EE/ES-endo or EE/ES-hydro. In the secretory phase ES-endo without autophagy inhibition, IL-1 beta and TNF alpha secretion were significantly higher compared with those of ES-healthy after stimulation with either LPS or poly I:C for 4 h (P < 0.001) and for 24 h (P < 0.01). Conclusion: Pathogen-induced autophagy was impaired in EE/ES-endo. Increased IL-1 beta and TNF alpha release in response to pathogenic triggers in the secretory phase ES-endo may result in the development of an inflammatory uterine microenvironment detrimental to successful embryo implantation.

One of the major problems of success in infertility treatment could depend on the understanding how the potential factors may affect the conception. The aim of this study was to evaluate present understanding of such factors or hormonal causes that may induce infertility. We studied the interactions between the two menstrual cycle hormones i.e., cortisol (COR) and prolactin (PRL), along with the ultrasonographic ovulation parameters in a group of N = 205 women with diagnosed infertility. The control group consisted of N = 100 women with confirmed fertility. In both groups, follicle-stimulating hormone (FSH), luteinizing hormone (LH), anti-Mullerian hormone (AMH), thyroid stimulating hormone (TSH), PRL, COR were examined on the third day of the cycle, and estradiol (E2), progesterone (P), and COR were examined during ovulation and 7-days afterwards. In the infertile group, higher levels of PRL and COR were observed than that of in the control group. Cortisol levels at all phases of the menstrual cycle and PRL negatively correlated with E2 secretion during and after ovulation, thus contributed to the attenuation of the ovulatory LH surge. Infertile women who conceived presented with higher levels of E2 during and after ovulation, higher P after ovulation, and thicker endometrium than that of the women who failed to conceive. In conclusion, elevated secretion of COR and PRL in infertile women impairs the menstrual cycle by decreasing the pre-ovulatory LH peak and E2 and postovulatory E2 levels that affect the endometrial growth, and consequently reduce the chances to conceive.