Immune-inflammation gene signatures in endometriosis patients

• Published in: Fertility and sterility Vol. 106; no. 6; pp. 1420 - 1431.e7
• Main Authors: Ahn, Soo Hyun, Khalaj, Kasra, Young, Steven L., Lessey, Bruce A., Koti, Madhuri, Tayade, Chandrakant
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2016
• Subjects: Angiogenesis; Apoptosis - genetics; Case-Control Studies; Cell Adhesion - genetics; Chemotaxis - genetics; Cluster Analysis; Cytokines - genetics; Cytokines - immunology; Cytotoxicity, Immunologic - genetics; endometriosis; Endometriosis - diagnosis; Endometriosis - genetics; Endometriosis - immunology; Endometrium - immunology; Endometrium - pathology; Female; Gene Expression Profiling; Genetic Markers; Hospitals, Teaching; Humans; immune genes; infertility; inflammation; Inflammation - diagnosis; Inflammation - genetics; Inflammation - immunology; Internal Medicine; Lymphocyte Activation - genetics; Obstetrics and Gynecology; Receptors, Cytokine - genetics; Receptors, Cytokine - immunology; Transcriptome; endometriosis; Angiogenesis; immune genes; infertility; inflammation
• DOI: 10.1016/j.fertnstert.2016.07.005
• ISSN: 0015-0282

To determine if the molecular profiles of endometriotic lesions contain informative measures of inflammation and immune dysfunction that may contribute to better understanding of the interplay between immune dysfunction and inflammation and their contribution to endometriosis pathogenesis. Immune and inflammation transcriptomic analysis with the use of the Nanostring nCounter GX Human Immunology V2 platform (579 human immune and inflammation–related genes and 15 housekeeping genes). Academic university and teaching hospital. None. Stage III–IV endometriosis patients with infertility (n = 8) and fertile disease-free control women undergoing tubal ligation (n = 8). Menstrual stage was matched to secretory phase in all participants. Immune and inflammation transcriptomics quantification from ectopic endometriotic lesions and matched eutopic endometrium from patients. Endometria of fertile women served as control subjects. Our results displayed endometriotic lesions as molecularly distinct entities compared with eutopic endometrium and endometrium of control samples; 396 out of 579 screened immune and inflammation–related genes were significantly different in ectopic tissues compared with control endometrium. Most importantly, eutopic endometrium of the patients displayed a unique molecular profile compared with the control endometrium (91/579 genes were significantly different), particularly of genes involved in regulation of cell apoptosis and decidualization. We characterize differential expression of immune-inflammation genes in endometriosis patients, and show molecular distinction of eutopic endometrium of patients compared with control fertile women.