NDLI: IL-17A Contributes to the Pathogenesis of Endometriosis by Triggering Proinflammatory Cytokines and Angiogenic Growth Factors.

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IL-17A Contributes to the Pathogenesis of Endometriosis by Triggering Proinflammatory Cytokines and Angiogenic Growth Factors.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Edwards, Andrew K. Singh, Sukhbir S. Lessey, Bruce A. Ahn, Soo Hyun Tayade, Chandrakant Young, Steven L.
Description	Author Affiliation: Ahn SH ( Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada); Edwards AK ( Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada); Singh SS ( Department of Obstetrics and Gynecology, University of Ottawa, Ottawa, Ontario K1H 7W9, Canada); Young SL ( Department of Obstetrics and Gynecology, University of North Carolina, Chapel Hill, NC 27514); Lessey BA ( Department of Obstetrics and Gynecology, Greenville Health System, Greenville, SC 29605.); Tayade C ( Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada)
Abstract	Endometriosis is a chronic, inflammatory disease characterized by the growth of endometrial tissue in aberrant locations outside the uterus. Neoangiogenesis or establishment of new blood supply is one of the fundamental requirements of endometriotic lesion survival in the peritoneal cavity. IL-17A is emerging as a potent angiogenic and proinflammatory cytokine involved in the pathophysiology of several chronic inflammatory diseases such as rheumatoid arthritis and psoriasis. However, sparse information is available in the context of endometriosis. In this study, we demonstrate the potential importance of IL-17A in the pathogenesis and pathophysiology of endometriosis. The data show a differential expression of IL-17A in human ectopic endometriotic lesions and matched eutopic endometrium from women with endometriosis. Importantly, surgical removal of lesions resulted in significantly reduced plasma IL-17A concentrations. Immunohistochemistry revealed localization of IL-17A primarily in the stroma of matched ectopic and eutopic tissue samples. In vitro stimulation of endometrial epithelial carcinoma cells, Ishikawa cells, and HUVECs with IL-17A revealed significant increase in angiogenic (vascular endothelial growth factor and IL-8), proinflammatory (IL-6 and IL-1ß), and chemotactic cytokines (G-CSF, CXCL12, CXCL1, and CX3CL1). Furthermore, IL-17A promoted tubulogenesis of HUVECs plated on Matrigel in a dose-dependent manner. Thus, we provide the first evidence, to our knowledge, that endometriotic lesions produce IL-17A and that the removal of the lesion via laparoscopic surgery leads to the significant reduction in the systemic levels of IL-17A. Taken together, our data show a likely important role of IL-17A in promoting angiogenesis and proinflammatory environment in the peritoneal cavity for the establishment and maintenance of endometriosis lesions.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1501138
Journal	The Journal of Immunology
Issue Number	6
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-09-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Endometriosis Immunology Endometrium Pathology Surgery Interleukin-17 Neovascularization, Pathologic Cell Line Chemokine Cx3cl1 Biosynthesis Chemokine Cxcl1 Chemokine Cxcl12 Endometrial Neoplasms Metabolism Blood Supply Granulocyte Colony-stimulating Factor Human Umbilical Vein Endothelial Cells Inflammation Blood Interleukin-1beta Interleukin-6 Interleukin-8 Laparoscopy Vascular Endothelial Growth Factor A Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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IL-17A Contributes to the Pathogenesis of Endometriosis by Triggering Proinflammatory Cytokines and Angiogenic Growth Factors.

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IL-17A Contributes to the Pathogenesis of Endometriosis by Triggering Proinflammatory Cytokines and Angiogenic Growth Factors.