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
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Endometriosis serum from women with low sIL-1RII levels induced increased monocyte MCP-1 secretion, which recombinant sIL-1RII blocked, suggesting a deficiency in IL-1 down-regulation.
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Abstract
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-1beta, and IL-1alpha 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-1beta and IL-1alpha 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.
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Courtesy of the U.S. National Library of Medicine
Courtesy of the U.S. National Library of Medicine