Inflammatory cytokines differentially up-regulate human endometrial haptoglobin production in women with endometriosis  

Oleh:

Sharpe-Timms, K.L. ; Nabli, H. ; Zimmer, R.L.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Human Reproduction vol. 25 no. 05 (May 2010), page 1241-1250.
Topik: cytokines; endometrium; haptoglobin; endometriosis

Ketersediaan

Perpustakaan FK Nomor Panggil: H07.K.2010.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

BACKGROUND Evidence suggests that eutopic endometrium from women with endometriosis (US-E) has intrinsic functional anomalies compared with women without endometriosis (US-C). We hypothesized that differences in endometrial haptoglobin (eHp) mRNA and protein levels exist between eutopic endometrium from US-E and US-C and that inflammatory mediators may be involved. METHODS Endometrial stromal cells and tissue explants from US-E (n = 18) and US-C (n = 18) were cultured (24 h/48 h for cells/explants) with interleukin (IL)-1a, -1ß, -6, -8 or tumor necrosis factor-alpha (TNF-a) at 0–100 ng/ml. eHp protein in media and mRNA levels were quantified by enzyme-linked immunosorbent assay and quantitative PCR. RESULTS In eutopic endometrial stromal cells from US-E, IL-1ß, IL-6 and TNF-a (10 ng/ml) increased eHp mRNA levels (P = 0.002, P < 0.001 and P < 0.001, respectively) and eHp protein (P = 0.023, 0.031 and 0.006, respectively) versus control. In endometrial tissues from US-E, IL-1ß, IL-6 and TNF-a increased eHp mRNA (P < 0.001, P = 0.017 and P < 0.001, respectively) and eHp protein (P < 0.001, P = 0.007 and 0.039, respectively) versus control. IL-1a and IL-8 had small or no effects on isolated endometrial cells or tissues. In US-C, IL-1ß, IL-8 and TNF-a each reduced eHp mRNA in endometrial stromal cells (all P < 0.001) versus control; IL-1a and IL-6 had no effect. eHp mRNA increased in endometrial tissues from US-C in response to IL-1ß (P = 0.008), IL-6 (P = 0.015) and TNF-a (P = 0.031) versus control; IL-1a or IL-8 had no effect. CONCLUSIONS Endometrium from US-E differentially responds to specific inflammatory cytokines by production of eHp. We propose that up-regulation of endometrial eHp by inflammatory mediators disrupts normal endometrial function and may facilitate the pathogenesis of endometriosis.

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