Women with interleukin-1 beta levels in quintiles 2-4 had a higher risk of endometriosis (for the second quintile, relative risk (RR) = 3.30, 95% confidence interval (CI): 1.06, 10.3; for the third quintile, RR = 3.36, 95% CI: 1.09, 10.4; and for the fourth quintile, RR = 4.64, 95% CI: 1.58, 13.6; P for trend = 0.62), which suggested an association beginning at 0.47 pg/mL or greater.
In endometriosis, TGF-β could affect differentiation of T helper (Th) cells, hence produce more IL-17 and IL-10 to PF and might have an indirect influence on inflammation, which is associated with higher IL-1β and IL-6 levels.
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.
This points to a deficiency in the local control of IL-1 that, in view of the cytokine's elevated levels and potent proinflammatory, angiogenic, and growth-promoting effects, may contribute to endometriosis development.
The PR-B/A ratio was measured via real-time polymerase chain reaction after in vitro culture, in which endometrial cells were treated with either tumor necrosis factor-alpha (TNF-α), interleukin-1 beta, or peritoneal fluid obtained from women with advanced-stage endometriosis.
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.
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.
The imbalance between IL-1α, pro-IL-1β, mature IL-1β and sIL-1R2 and sIL-1RAcP in the peritoneal fluid and serum of women with endometriosis may be linked to the ability of transforming an acute inflammation into a chronic one.
Correlation analysis showed that the gene expression levels of hBD-2 in the ectopic and eutopic endometrium of EMS patients were positively correlated with the gene expression levels of IL-1β and TNF-α (P < 0.01).
To evaluate the effects of IL-1β on Ninj1 gene expression in endometriosis, ESCs isolated from ovarian endometrioma (n = 5) were treated with IL-1β (5 ng/mL) for 3 or 6 hours.
LXA<sub>4</sub> may inhibit the progression of endometriosis partly by lowering or raising the effect of IL-1β, mediated via some inflammation-related proteins (e.g. vinculin) and immune response-related protein (e.g.IL-4) in vitro.
In the follicular fluid, IL-1β and IL-6 showed significantly (P < 0.001 and 0.01, respectively) higher median concentrations in the endometriosis group than in the control group and a tendency towards endometriosis severity (rAFS stage) dependence.
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.
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.