In view of the wide spectrum of IL-1 inflammatory and growth-promoting effects, downregulation of sIL1RAcP, which is known for inhibiting IL1, indicates a profound defect in the capability of endometrial cells of women with endometriosis to counterregulate IL-1 effects and may represent an important mechanism underlying the ability of these cells to implant and develop into host tissues.
Effect of vascular endothelial growth factor and interleukin-1beta on apoptosis in endometrial cell cultures from patients with endometriosis and controls.
Case-control study to investigate the association between endometriosis and four inflammation-related genes: interleukin (IL)-6, IL-10, IL-1 beta, and cyclooxygenase-2.
This study suggests the involvement of the nuclear transcription factor NF-kappaB in MIF gene activation in ectopic endometrial cells in response to IL-1 beta and identifies a possible pathway of endometriosis-associated inflammation and ectopic cell growth.
These results suggest that IL-1RII can neutralize IL-1 beta and counteract its effect on endometrial stromal cells, and may provide a new clinical strategy for the treatment of endometriosis.
These results, along with recent findings that TSA suppresses proliferation, interleukin-1 beta-induced cyclo-oxygenase 2 expression, and constitutive or TNFalpha-stimulated nuclear factor kappa B activation in endometrial and endometriotic cells, makes histone deacetylase inhibitors a promising class of compounds for novel and more effective medical treatment of endometriosis, especially given the mounting evidence that endometrios be an epigenetic disease.
The reduced levels of IL-1RII mRNA in the endometrium of women suffering from endometriosis reveals a profound defect in IL-1RII gene expression and, consequently, a reduced capability of endometrial tissue to down-regulate IL-1 activity.
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.
Activated peritoneal macrophages are associated with endometriosis and may play a central role in its aetiology by releasing interleukin-1beta (IL-1beta) in response to refluxed endometrium.
Our results suggest that peritoneal macrophages express IL-1ra mRNA rather than IL-1 beta mRNA with the progress of endometriosis and that peritoneal macrophages may secrete IL-1ra protein that modulates the effects of IL-1.