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Interleukin‐17A expression in endometriotic tissue and plasma samples from women with endometriosis (539.2)
Author(s) -
Ahn Soo,
Edwards Andrew,
Nakamura Diane,
Lessey Bruce,
Tayade Chadrakant,
Reifel Conrad
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.539.2
Subject(s) - endometriosis , pathogenesis , proinflammatory cytokine , flow cytometry , medicine , stromal cell , cancer research , pathology , inflammation , immunology
Cytokines present within the environment of endometriosis are believed to contribute to the pathogenesis of the disease by promoting inflammatory conditions surrounding the implantation of endometriotic lesions. Interleukin‐17A is a member of proinflammatory cytokines implicated in the pathogenesis of various chronic inflammatory diseases. However, its role in the disease progression of endometriosis is poorly understood. The objective of this study was to elucidate the involvement of IL‐17A in the pathogenesis of endometriosis. To investigate this, IL‐17A concentration was measured in plasma, eutopic and ectopic samples from women with endometriosis and in plasma and eutopic samples from women without endometriosis. Immunostaining for IL‐17A was conducted on eutopic and ectopic tissue sections. To elucidate biological function of IL‐17A, WST‐1 proliferation assay, cell cycle analysis with Propidium Iodide (PI) , and supernatant analysis were performed with endometrial epithelial carcinoma cells (EECCs) . Expression of IL‐17A, IL‐17RA, and IL‐17RC mRNA from EECCs and primary EECs was measured using qPCR. Flow cytometry was performed on EECCs to detect IL‐17RA expression. Results show presence of IL‐17A in plasma samples and ectopic tissue samples from women with endometriosis. Imunohistochemistry confirmed the presence of IL‐17A positive cells within both the epithelium and stroma of eutopic and ectopic tissue sections. Even though IL‐17A has shown no proliferative or apoptotic effect on EECCs, its stimulation on EECCs induced increased production of G‐CSF, VEGF, PDGF‐AA, and SDF‐1. Follow up investigation is needed to elucidate the understanding of the relationship between the presence of IL‐17A and the pathogenesis of endometriosis. Grant Funding Source : Supported by CIHR