Evaluation of the content and the pathogenetic role of cytokines in the peritoneal fluid in patients with deep infiltrative endometriosis
Deep infiltrative endometriosis is associated with significantly altered levels of IL-2, IL-6, IL-10, IL-33, MCP-1, IP-10, FGF, and TGF-β in peritoneal fluid, correlating with pain severity.
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The study evaluated peritoneal fluid levels of selected pro- and anti-inflammatory cytokines, chemokines, and growth factors in 120 women with deep infiltrative endometriosis, compared with 20 controls without gynecologic disease, using IFA or flow cytometry-based assays. The authors found markedly reduced IL-2 and IL-10, increased IL-6 and IL-33 (with IL-33 and IL-6 linked to pain severity), decreased IP-10, increased MCP-1, increased FGF, and reduced TGF-β in patients versus controls. A key limitation stated in the paper is that the control group was smaller and limited to women undergoing assessment for IVF for male-factor infertility, which may not fully match broader pelvic inflammatory or pain-related contexts. This paper is centrally about endometriosis — specifically deep infiltrative endometriosis and cytokine/chemokine alterations in peritoneal fluid and their proposed pathogenetic role.
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References (7)
- Chronic pelvic pain in women: etiology, pathogenesis and diagnostic approach via openalex
- Increased levels of interleukin-6 and interleukin-10 in the peritoneal fluid of patients with endometriosis via openalex
- Interleukin-6 and other soluble factors in peritoneal fluid and endometriomas and their relation to pain and aromatase expression via openalex
- Monocyte chemotactic protein-1 concentration in peritoneal fluid of women with endometriosis and its modulation of expression in mesothelial cells via openalex
- Peritoneal fluid interleukin-6 in women with chronic pelvic pain via openalex
- TGF- 1 induces proteinase-activated receptor 2 (PAR2) expression in endometriotic stromal cells and stimulates PAR2 activation-induced secretion of IL-6 via openalex
- W2171069248 via openalex
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