Correlation Between Decreased Type‐II Interleukin‐1 Receptor and Increased Monocyte Chemotactic Protein‐1 Expression in the Endometrium of Women with Endometriosis
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Decreased expression of IL-1 receptor type II correlates with increased monocyte chemotactic protein-1 in the endometrium of women with endometriosis, particularly in early stages and across the menstrual cycle.
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Abstract
PROBLEM: Monocyte chemotactic protein-1 (MCP-1), a potent inducer of macrophage recruitment and activation, is overexpressed in the eutopic endometrium of women with endometriosis. Eutopic endometrial cells of women with endometriosis secrete higher levels of MCP-1 than those of normal women, following stimulation with interleukin-1 (IL-1). The aim of this study was to examine whether there is any correlation between the expression of IL-1 receptor type II (IL-IRII), a specific downregulator of IL-1 activity, and that of MCP-1 in the eutopic endometrium of women with endometriosis. METHOD OF STUDY: Endometrial biopsies of 46 women with endometriosis and 22 healthy women were evaluated simultaneously for IL-1RII and MCP-1 expression by immunohistochemistry. RESULTS: Our study revealed a highly significant correlation between the decreased expression of IL-1RII and the increased expression of MCP-1 in the endometrial tissue of women with endometriosis (Spearman correlation coefficient r = -0.377, P = 0.002), particularly in the initial stages of the disease (stages I and II; r = - 0.368, P = 0.020 and r = -0.480, P = 0.002, respectively). Furthermore, this correlation was observed in the proliferative (r = -0.366, P = 0.047) and the secretory phases (r = -0.321, P = 0.049) of the menstrual cycle. CONCLUSIONS: These results suggest that the reduced capability of endometrial tissue to downregulate IL-1 proinflammatory effects may be involved in the increased expression of MCP-1 in the endometrium of women with endometriosis and the establishment of an inflammatory state. The results also indicate a sustained process of cell activation throughout the menstrual cycle.
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Cited by (15)
- Therapeutic Mechanism and Clinical Observation of Traditional Chinese Medicine Combined with Interventional Recanalization for Tubal Infertility 2021
- Cross-disorder analysis of endometriosis and its comorbid diseases reveals shared genes and molecular pathways and proposes putative biomarkers of endometriosis 2019
- Endometrial biomarkers for the non-invasive diagnosis of endometriosis 2016
- Identifying biomarkers for non-invasive diagnosis of endometriosis 2016
- Can chemokines be used as biomarkers for endometriosis? A systematic review 2013
- Interleukin-1β induces cyclooxygenase-2 expression and promotes the invasive ability of human mesenchymal stem cells derived from ovarian endometrioma 2011
- Endometrioid ovarian cancer and endometriotic cells exhibit the same alteration in the expression of interleukin-1 receptor II: To a link between endometriosis and endometrioid ovarian cancer 2010
- Expression of interleukin-1 (IL-1) ligands system in the most common endometriosis-associated ovarian cancer subtypes 2010
- Avaliação das concentrações das interleucinas 1-beta e 6 e da proteína amilóide A, no líquido peritoneal e no soro de pacientes com endometriose pélvica 2007
- Polymorphisms in Exons 1B and 1C of the Type I Interleukin‐1 Receptor Gene in Patients with Endometriosis 2006
- Concentrations of interleukin (IL)-1α, IL-1 soluble receptor type II (IL-1 sRII) and IL-1 receptor antagonist (IL-1 Ra) in the peritoneal fluid and serum of infertile women with endometriosis 2005
- Decreased levels of interleukin-18 in peritoneal fluid but not in serum of patients with endometriosis 2004
- Relationship between apoptosis and the number of macrophages in eutopic endometrium from women with and without endometriosis 2002
- 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 2002
- Abnormal Interleukin-1 Receptor Type II Gene Expression in the Endometrium of Women with Endometriosis1 2002
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