Adult ; Endometriosis ; complications ; metabolism ; Endometrium ; metabolism ; Female ; Humans ; Infertility, Female ; etiology ; metabolism ; Leptin ; metabolism

Endometriosis, a heterogeneous, inflammatory, and estrogen-dependent gynecological disease defined by the presence and growth of endometrial tissues outside the lining of the uterus, affects approximately 5-10% of reproductive-age women, causing chronic pelvic pain and reduced fertility. Although the etiology of endometriosis is still elusive, emerging evidence supports the idea that immune dysregulation can promote the survival and growth of retrograde endometrial debris. Peritoneal macrophages and natural killer (NK) cells exhibit deficient cytotoxicity in the endometriotic microenvironment, leading to inefficient eradication of refluxed endometrial fragments. In addition, the imbalance of T-cell subtypes results in aberrant cytokine production and chronic inflammation, which contribute to endometriosis development. Although it remains uncertain whether immune dysregulation represents an initial cause or merely a secondary enhancer of endometriosis, therapies targeting altered immune pathways exhibit satisfactory effects in preventing disease onset and progression. Here, we summarize the phenotypic and functional alterations of immune cells in the endometriotic microenvironment, focusing on their interactions with microbiota and endocrine and nervous systems, and how these interactions contribute to the etiology and symptomology of endometriosis.
Female ; Humans ; Endometriosis/metabolism* ; Killer Cells, Natural/metabolism* ; T-Lymphocytes/metabolism* ; Estrogens ; Endometrium/metabolism*

Cytokines ; immunology ; Embolism ; immunology ; metabolism ; pathology ; Endometriosis ; immunology ; metabolism ; pathology ; Female ; Hormones ; metabolism ; Humans

Endometriosis ; etiology ; metabolism ; Environmental Pollution ; Female ; Hormones ; metabolism ; Humans ; Receptors, CCR ; metabolism

In order to investigate the mechanism of elevated vascular endothelial growth factor (VEGF) in peritoneal fluids from patients with endometriosis, macrophages were recovered from peritoneal fluids obtained at the time of diagnostic laparoscopy from infertile women with endometriosis (EMT group, n=20) and without endometriosis (control group, n=20). Macrophages were cultured in vitro. The VEGF levels of peritoneal fluid and the supernatant of macrophages culture were determined by enzyme linked immunoassay (ELISA). Meanwhile, the eutopic (n=20) and ectopic endometrium (n=20) from endometriosis patients, and normal edometrium (n=20) from non-endometriosis patients were obtained for the analysis of VEGF expression by labeled Streptavidin Biotin (LSAB). It was found that VEGF levels in peritoneal fluid and macrophages culture supernatant were significantly higher in EMT group than in control group (P<0.01). In normal endometrium, VEGF showed a cyclic changes and similar in eutopic and ectopic endometrium from patients with endometriosis. There was no difference in the intensity of VEGF in endometrium between two groups within each menstrual phase. It is suggested that altered VEGF production by peritoneal macrophages and ectopic endometrium secretion may contribute to the elevated VEGF levels in the peritoneal fluid of patients with endometriosis.
Ascitic Fluid/*metabolism ; Cells, Cultured ; Endometriosis/*metabolism ; Macrophages, Peritoneal/pathology ; Vascular Endothelial Growth Factor A/*biosynthesis

A large number of studies have shown that the oxidative imbalance is common in patients with endometriosis. Abnormal respiratory chain of mitochondrial, estrogen metabolism imbalance, iron overload, and ectopic foci may increase active oxygen, reduction of antioxidant enzyme and non-enzymatic substances may result in decreased antioxidant level, and the exposure to environmental hazards may further aggravate oxidative imbalance in patients with endometriosis. This article analyzes the oxidative imbalance and its role in the pathogenesis of endometriosis from the aspects of excessive oxide production and decreased antioxidant capacity.
Antioxidants ; metabolism ; Endometriosis ; physiopathology ; Female ; Humans ; Oxidative Stress ; Reactive Oxygen Species ; metabolism

Adult ; Ascitic Fluid ; metabolism ; Endometriosis ; blood ; metabolism ; Female ; Humans ; Interleukin-18 ; analysis ; blood ; Middle Aged

Endometriosis is a common disease of reproductive age women and infertility is one of its clinical manifestations. Infertility of patients with severe endometriosis may be attributed to the anatomy alteration of pelvis.However, the infertility of patients with minimal to mild endometriosis whose pelvic anatomy remains intact is still hard to explain. It is considered that the infertility of patients with ninimal to mild endometriosis is associated with the alteration of the pelvic microenvironment. Several kinds of cytokines and proteins are involved in this process. They may disturb steps necessary to achieve successful pregnancy, such as ovulation,gamete transport, fertilization, embryo transport and implantation. Any disturbance to one of the steps mentioned above may lead to pregnant loss.
Cytokines ; metabolism ; Endometriosis ; complications ; metabolism ; pathology ; Female ; Humans ; Infertility, Female ; etiology ; metabolism ; Nitric Oxide Synthase ; metabolism ; Pregnancy

OBJECTIVETo detect the expression of fragile histidine triad in endometriosis and investigate the pathogenesis of endometriosis.

METHODSimmunohistochemistry was used to examine the expression of Fhit in the eutopic and ectopic endometria of 58 patients with endometriosis and in the endometria in 15 patients with hysteromyoma.

RESULTSThe intensity of Fhit expression decreased in the order of normal endometrium, eutopic endometrium in endometriosis group, and ectopic endometrium. In patients with endometriosis, Fhit expression in the eutopic and ectopic endometria in proliferative phase showed no significant difference from that in secretory phase (P>0.05). Fhit expression in the ectopic endometrium showed significant difference between different r-AFS stages. MOD of ectopic endometrium in stages I-II was significantly higher than that in stages III-IV (P<0.05), but Fhit expression in the eutopic endometrium showed no significant difference (P>0.05). MOD of ovarian endometriosis showed no difference with that of adenomyosis.

CONCLUSIONSFhit may play an important role in the development of endometriosis.

Acid Anhydride Hydrolases ; metabolism ; Adult ; Endometriosis ; metabolism ; pathology ; Endometrium ; metabolism ; Female ; Humans ; Middle Aged ; Neoplasm Proteins ; metabolism

BACKGROUNDStathmin was identified as an endometriosis-related protein by comparative proteomics in our previous study. As a microtubule-destabilizing factor, stathmin was shown to participate in the relay and integration of diverse intracellular signaling pathways involved in cell proliferation, differentiation, and many other cellular activities. To investigate whether stathmin is involved in the pathogenesis of endometriosis, we examined the expression of stathmin in eutopic endometrium of women with or without endometriosis.

METHODSEutopic endometrium samples were collected from thirty-six patients who were diagnosed as endometriosis and the nineteen age-matched patients who were confirmed to be free of endometriosis surgically and histologically. The expression of stathmin mRNA was detected by real-time PCR, and its protein was detected by Western blotting and immunohistochemistry.

RESULTSStathmin was overexpressed in eutopic endometrium of women with endometriosis detected by real-time PCR in mRNA levels and by Western blotting in protein levels, without significant difference between proliferative and secretory phase. Immunohistochemistry showed that stathmin protein was localized in both endometrial glandular and stromal cells throughout the menstrual cycle.

CONCLUSIONSStathmin is overexpressed in endometrium of patients with endometriosis and may play a role in the pathogenesis of endometriosis.

Adult ; Blotting, Western ; Endometriosis ; metabolism ; Endometrium ; metabolism ; Female ; Humans ; Immunohistochemistry ; Middle Aged ; Polymerase Chain Reaction ; Stathmin ; genetics ; metabolism