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...
Gespeichert in:
Veröffentlicht in: | Fertility and sterility 2002-10, Vol.78 (4), p.836-842 |
---|---|
Hauptverfasser: | , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
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 |