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ArtikelExpression of interleukin-8 and monocyte chemotactic protein 1 in women with endometriosis  
Oleh: Ulukus, Murat ; Ulukus, E. Cagnur ; Goker, Ege N. Tavmergen
Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 91 no. 03 (Mar. 2009), page 687-693 .
Topik: Endometriosis; endometrium; immunohistochemistry; interleukin-8; monocyte chemotactic protein 1
Ketersediaan
  • Perpustakaan FK
    • Nomor Panggil: F02.K.2009.01
    • Non-tandon: 1 (dapat dipinjam: 0)
    • Tandon: tidak ada
    Lihat Detail Induk
Isi artikelObjective To investigate the expression and localization of interleukin-8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) in women with and without endometriosis. Design Comparative immunohistochemical study. Setting Academic medical center. Patient(s) Ectopic (n = 24) and homologous eutopic endometrium (n = 24) from women with endometriosis and endometrium from women without endometriosis (n = 27) were used for immunohistochemical analysis of IL-8 and MCP-1. Intervention(s) Tissue sections were immunostained with antihuman IL-8 and MCP-1 antibodies. Main Outcome Measure(s) Microscopic evaluation to assess the presence and localization of IL-8 and MCP-1 throughout the menstrual cycle in both eutopic endometrial and endometriotic tissues of women with endometriosis and comparison with normal endometrium. Result(s) In normal endometrium, secretory phase samples expressed higher levels of epithelial IL-8 than in proliferative phase samples. Epithelial MCP-1 expression was similar in both proliferative and secretory phases. Proliferative phase samples showed higher epithelial IL-8 and MCP-1 expressions in eutopic endometrium of women with endometriosis compared with that of normal women. Immunoreactivities of both chemokines were significantly increased in the epithelial cells of ectopic endometrial tissues compared with those of normal endometrium. Conclusion(s) These findings suggest that IL-8 and MCP-1 may be involved in the pathogenesis of endometriosis.
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