{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T13:18:23Z","timestamp":1787318303108,"version":"build-2736575974"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2022,5,12]],"date-time":"2022-05-12T00:00:00Z","timestamp":1652313600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/501100020309","name":"KARL STORZ SE & Co. 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However, the underlying mechanisms of the establishment of non-resolving, low-grade inflammation in endometriosis remain to be clarified.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>STUDY DESIGN, SIZE, DURATION<\/jats:title>\n                    <jats:p>Endometrial and\/or endometriotic samples of 60 patients who had histological evidence of deep endometriosis and endometrial samples from 32 healthy fertile women were analyzed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>PARTICIPANTS\/MATERIALS, SETTING, METHODS<\/jats:title>\n                    <jats:p>The effects of priming with ligands of Toll-like receptors (TLRs) 2, 3 and 4 on secretion of inflammatory mediators (tumor necrosis factor-\u03b1, C-X-C motif chemokine ligand-10 [CXCL-10], IL6 and IL-10) after a second challenge with TLR ligands in endometrial and endometriotic stromal cells were investigated. Then, the effects of IL-6\/soluble (s) IL-6 receptor (R)\/STAT3 signaling, as well as inhibition of STAT3 activation by knockdown of STAT3 or pharmacological inhibition (S3I-201), on the pro-fibrotic phenotype in endometrial and endometriotic stromal cells in vitro were investigated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>MAIN RESULTS AND THE ROLE OF CHANCE<\/jats:title>\n                    <jats:p>Priming with TLR ligands for 4\u2009h had no significant effects, whereas 24\u2009h of priming significantly decreased secretion of IL-6, after a second challenge in endometrial stromal cells of healthy women. In endometriotic stromal cells, whereas 24\u2009h of priming had no significant effects, priming with TLR ligands for 4\u2009h significantly increased secretion of IL-6 after a second challenge. IL-6\/soluble IL-6 receptor (sIL-6R) induced a pro-fibrotic phenotype (cell proliferation, collagen type I synthesis, \u03b1-smooth muscle actin positive stress fibers, cell migration and collagen gel contraction) as well as nuclear factor-kappa B (NF-\u03baB) activation of endometriotic stromal cells. In contrast, IL-6\/sIL-6R had no significant effects on either a pro-fibrotic phenotype or NF-\u03baB activation of endometrial stromal cells of healthy women. Stimulation with transforming growth factor (TGF)-\u03b21 and\/or IL-6\/sIL-6R for 1\u2009h and 48\u2009h activated STAT3, but induced very low or no suppressor of cytokine signaling (SOCS) 1 and 3 protein expression in endometriotic stromal cells. In endometrial stromal cells of healthy women, IL-6\/sIL-6R-induced STAT3 and SOCS1\/3 expression at 1\u2009h, whereas no STAT3 activation was detected at 48\u2009h. Knockdown of STAT3 gene or S3I-201 (a STAT3 inhibitor) decreased the IL-6\/sIL-6R-induced pro-fibrotic phenotype as well as NF-\u03baB activation and TGF-\u03b21-induced cell proliferation of endometriotic stromal cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>LARGE SCALE DATA<\/jats:title>\n                    <jats:p>N\/A.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>LIMITATIONS, REASONS FOR CAUTION<\/jats:title>\n                    <jats:p>In vivo studies are required to confirm the present in vitro results. However, it remains challenging to mimic non-resolving chronic inflammation in animal models, as active inflammation can resolve spontaneously.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>WIDER IMPLICATIONS OF THE FINDINGS<\/jats:title>\n                    <jats:p>Dysfunction of negative regulators of IL-6\/sIL-6R\/STAT3 signaling may cause persistent activation of STAT3 in endometriosis. Since STAT3 activation in the endometrium is essential for successful embryo implantation, treatment with STAT3 inhibitors would not be appropriate for women wishing to conceive. However, targeting impaired negative regulation of IL-6\/sIL-6R\/STAT3 signaling may still represent a promising avenue for the treatment of endometriosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>STUDY FUNDING\/COMPETING INTEREST(S)<\/jats:title>\n                    <jats:p>This study was supported in part by the KARL STORZ SE &amp; Co. KG (Tuttlingen, Germany). There are no conflicts of interest.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/humrep\/deac098","type":"journal-article","created":{"date-parts":[[2022,4,25]],"date-time":"2022-04-25T15:11:39Z","timestamp":1650899499000},"page":"1489-1504","source":"Crossref","is-referenced-by-count":35,"title":["Persistent activation of signal transducer and activator of transcription 3 via interleukin-6 trans-signaling is involved in fibrosis of endometriosis"],"prefix":"10.1093","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9297-6515","authenticated-orcid":false,"given":"Sachiko","family":"Matsuzaki","sequence":"first","affiliation":[{"name":"CHU Clermont-Ferrand, Chirurgie Gyn\u00e9cologique , Clermont-Ferrand, France"},{"name":"Universit\u00e9 Clermont Auvergne, Institut Pascal, UMR6602, CNRS\/UCA\/SIGMA , Clermont-Ferrand, 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