Abstract
BackgroundA deficiency in the counter-regulatory mechanisms of interleukin 1 (IL1) may play a significant role in endometriosis pathogenesis and associated chronic inflammation. The aim of this study was to investigate peripheral blood levels of soluble IL1 receptor accessory protein (sIL1RAP), a potent natural inhibitor of IL1, in women with and without endometriosis.MethodsPeripheral blood samples were collected from women with endometriosis (n = 47) consulting for infertility, pelvic pain or tubal ligation, in whom the disease was diagnosed at laparoscopy. Control healthy women (n = 27) were requesting tubal ligation or reanastomosis and had no visible evidence of endometriosis at laparoscopy. sIL1RAP levels were determined by ELISA, whereas estradiol (E2) and progesterone (P4) levels were determined by competitive immunoassays.ResultssIL1RAP levels were significantly decreased in women with early endometriosis stages compared to controls (p < 0.05) and markedly during the proliferative phase of the menstrual cycle (p < 0.001). Actually, while sIL1RAP were significantly increased in the proliferative compared to the secretory phase in normal women (p < 0.0001) and peaked at the end of this phase, sIL1RAP remained consistently low and showed non-significant variations throughout the menstrual cycle in women with endometriosis.ConclusionsLower circulating levels of sIL1RAP points to a significant impairment in the counter-regulatory mechanisms of IL1, which in view of the cytokine’s potent inflammatory and growth-promoting properties may play a significant role in the pathophysiology of endometriosis.
Highlights
A deficiency in the counter-regulatory mechanisms of interleukin 1 (IL1) may play a significant role in endometriosis pathogenesis and associated chronic inflammation
Results soluble IL1 receptor accessory protein (sIL1RAP) was detected in the peripheral blood and the distribution of its concentrations in normal controls and women with endometriosis are presented in Figure 1. sIL1RAP levels were slightly decreased in women with endometriosis, but this decrease did not reach the level of statistical significance (p = 0.08) (Figure 1A)
Further distribution of sIL1RAP values along the menstrual cycle showed a peak, which, in normal women, was reached at the end of the proliferation phase. The amplitude of such a peak was significantly lower (p < 0.01) compared to normal controls, and no significant cycle-dependent changes could be observed (Figure 3B). Since these results suggest a hormonal regulation of sIL1RAP levels, we analysed E2 and P4 concentrations in the same serum samples
Summary
A deficiency in the counter-regulatory mechanisms of interleukin 1 (IL1) may play a significant role in endometriosis pathogenesis and associated chronic inflammation. Endometriosis is one of the most frequent gynaecological diseases in reproductive age women. Defined as an ectopic growth of endometrial tissue, endometriosis is frequently associated pelvic pain and infertility (30-40%) [1] and a chronic pelvic inflammation [2]. Cumulative evidence clearly points to a significant role for immune factors in endometriosis development. Inflammation is a major hallmark of endometriosis, but the underlying mechanisms are not clearly elucidated. Local immune surveillance appears to be deficient in women and exacerbate the inflammatory reaction via cyclical reflux of menstrual debris into the peritoneal cavity [3,4,5,6,7]
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