Soluble interleukin-1 receptor type II blocks monocyte chemotactic protein-1 secretion by u937 cells in response to peripheral blood serum of women with endometriosis

Objective: To assess the ability of peripheral blood serum from women with endometriosis to induce monocyte chemotactic protein-1 (MCP-1) secretion by monocytes and the putative role of the interleukin-1 (IL-1) system in endometriosis-associated monocyte activation. Design: Cultures of U937 monocyti...

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Veröffentlicht in:Fertility and sterility 2002-10, Vol.78 (4), p.836-842
Hauptverfasser: Kharfi, Abdelaziz, Akoum, Ali
Format: Artikel
Sprache:eng
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Zusammenfassung:Objective: To assess the ability of peripheral blood serum from women with endometriosis to induce monocyte chemotactic protein-1 (MCP-1) secretion by monocytes and the putative role of the interleukin-1 (IL-1) system in endometriosis-associated monocyte activation. Design: Cultures of U937 monocytic cells exposed to serum from normal women (control group) or women with endometriosis. Setting: Gynecology clinic and human reproduction research laboratory. Patient(s): Seventy-nine women with endometriosis and 38 control women with no evidence of endometriosis at laparoscopy. Intervention(s): Peripheral blood obtained a few days before laparoscopy. Main Outcome Measure(s): MCP-1 secretion in the culture medium and serum concentrations of soluble IL-1 receptor type II (sIL-1RII), IL-1β, and IL-1α by ELISA or by enzyme immunometric assay. Result(s): Serum concentrations of sIL-1RII were significantly lower in women with stage I–II endometriosis than in control women, whereas serum concentrations of IL-1β and IL-1α were comparable between the two groups. The serum of women with endometriosis induced higher secretion of MCP-1 by U937 cells than that of control women, particularly in the initial stages of endometriosis (stages I–II), and recombinant IL-1RII (rIL-1RII) significantly blocked that secretion. Conclusion(s): These findings point toward a deficiency in the mechanisms involved in the down-regulation of IL-1 actions at the systemic level and reveal sIL-1RII as a key factor involved in that process.
ISSN:0015-0282
1556-5653
DOI:10.1016/S0015-0282(02)03335-6