Association of the Precursor of Interleukin-1β and Peritoneal Inflammation—Role in Pathogenesis of Endometriosis

Abstract

Background: The most important proinflammatory cytokine is interleukin (IL)-1β, however its precursor, prointerleukin-1β (proIL-1β), can also potentiate inflammatory state. The aim of this study was to explore the involvement of proIL-1β in pathogenesis of endometriosis. For this purpose, we evaluated concentrations of proIL-1β, IL-1β, and soluble IL-1 receptor type 2 (sIL-1R2) in peritoneal fluid (PF) and macrophage culture medium of women with endometriosis. Methods: PF from 55 women with and without endometriosis was collected during laparoscopy. Peritoneal macrophages were cultured in basal and stimulated with lipopolysaccharide (LPS) conditions. Concentrations of cytokines were measured with enzyme-linked immunosorbent assays (ELISA). Results: PF proIL-1β and IL-1β levels in endometriosis women were higher than in the control. Higher basal and stimulated macrophage secretion of cytokines in endometriosis patients than in the control was observed. However, in endometriosis, there was a higher level of proIL-1β than for the mature molecule. Additionally, lower PF and macrophages culture medium sIL-1R2 levels were observed in women with endometriosis. Conclusions: Abnormal proIL-1β concentration in PF and higher macrophage secretion can escalate peritoneal inflammation and endometriosis formation. The results are presented as a total IL-1β, which is a sum of proIL-1β and IL-1β, and we believe that it reflects the actual cytokine production. The imbalance among all studied cytokines in endometriosis may be linked with an ability to transform acute inflammation to the chronic inflammation.