The Delicate Balance between the Good and the Bad IL-1 Proinflammatory Effects in Endometriosis

Curr Med Chem. 2018;25(18):2105-2121. doi: 10.2174/0929867325666180111093547.

Abstract

Background: Endometriosis is an inflammatory gynaecological disease with an associated chronic inflammation. Interleukin(IL)-1 is one of the most important immune and proinflammatory factors, produced mainly by monocytes and macrophages. Studies indicate the role of the cytokine from IL-1 family in endometrium-related disorders, particularly in endometriosis.

Methods: The information about the impact of cytokine from IL-1 cytokine family on the pathogenesis and development of endometriosis was obtained with an electronic literature search based on the PubMed and Medline databases, spanning the period of January 1950 to July 2017 and includes associated references in the published studies.

Results: The impairment of the IL-1 family cytokine-network may lead to changes in the activation of immune system in the peritoneal cavity of women with endometriosis. The aberrant ectopic endometrial cell properties of adhesion, implantation and proliferation may be the result of a reduced suppressive capacity controlling the IL-1. 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. Despite the fact that peritoneal macrophages secrete more antiinflammatory IL-1Ra and less proinflammatory IL-1 in the peritoneal cavity in affected women, the inflammation still develops.

Conclusions: This observation clearly suggested a significant inadequacy in the specific regulatory mechanisms of IL-1 activity at the peritoneal cavity level. The imbalance between all studied cytokines in endometriosis may escalate peritoneal inflammation and, in consequence, develop endometriosis.

Keywords: Endometriosis; inflammation; interleukin-1; interleukin-1 receptors; peritoneal fluid; serum..

Publication types

  • Review

MeSH terms

  • Endometriosis / physiopathology*
  • Female
  • Humans
  • Inflammation / chemically induced*
  • Interleukin 1 Receptor Antagonist Protein / metabolism
  • Interleukin-1 / metabolism*
  • Receptors, Interleukin-1 Type I / metabolism
  • Receptors, Interleukin-1 Type II / metabolism

Substances

  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1
  • Receptors, Interleukin-1 Type I
  • Receptors, Interleukin-1 Type II