title: Telocytes in Inflammatory Gynaecologic Diseases and Infertility.
abstract: Women suffered with inflammatory gynecologic diseases, such as endometriosis (EMs) and acute salpingitis (AS) often complained of sub- or infertility, even in those women without obvious macroscopic anatomical pelvic abnormalities also have unexplained infertility. Generally, besides the well-known impairment of classically described oviduct cells caused by inflammatory diseases, such as the ciliated cells, fibroblasts and myofibroblasts, the involvement of the newly identified telocytes (TCs) in disease-affected oviduct tissues and potential pathophysiological roles in fertility problems remain unknown. In this chapter, TCs was investigated in rat model of EMs- and AS-affected oviduct tissues. Results showed inflammation and ischaemia-induced extensive ultrastructural damages of TCs both in cellular body and prolongations, with obvious TCs loss and interstitial fibrotic remodelling. Such in vivo pathological alterations might contribute to structural and functional abnormalities of oviduct tissue and potentially engaged in sub- or infertility. And especially, TCs connected to various activated immunocytes in both normal and diseased tissues, thus might participate in local immunoregulation (either repression or activation) and serve a possible explanation for immune-mediated pregnancy failure. Then, in vitro cell co-culture study showed that uterine TC conditioned media (TCM) can activate mouse peritoneal macrophages and subsequently trigger its cytokine secretion, thus providepreliminary evidence that, TCs are not simply innocent bystanders, but are instead potential functional players in local immunoregulatory and immunosurveillance.
authors: Department of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow University, 188 Shizi Road, Suzhou City, Jiangsu Province, 215006, People's Republic of China. yang.xiaojun@hotmail.com.
authors: Xiao-Jun
authors: XJ
authors: Yang
mesh_terms: D000818:Animals; D018952:Antigens, CD34 / Q000235:genetics / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D004715:Endometriosis / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D005260:Female; D015870:Gene Expression; D006801:Humans; D007247:Infertility, Female / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D007249:Inflammation; D051379:Mice; D011247:Pregnancy; D011271:Pregnancy, Ectopic / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D012488:Salpingitis / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000067170:Telocytes / Q000378:metabolism / Q000473:pathology*; D000267:Tissue Adhesions / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D014599:Uterus / Q000378:metabolism / Q000473:pathology; D014746:Vimentin / Q000235:genetics / Q000378:metabolism
chemical_list: D018952:Antigens, CD34; D015415:Biomarkers; D014746:Vimentin
keywords: Acute salpingitis (AS); Cytokines; Endometriosis; Enzyme; Fertility disorder; Fibrosis; Immune response; Immunoregulation; Infertility; Inflammation; Inflammatory factors; Interstitial cells; Macrophage activation; Oviduct; Pelvic inflammatory disease; Rat model; Stromal cells; Tubal ectopic pregnancy; Tubal factor infertility; Uterine telocytes