The role of complement components C1q, MBL and C1 inhibitor in pathogenesis of endometriosis

Justyna Sikora1, Agnieszka Wróblewska-Czech2, Marta Smycz-Kubańska3

  • 1Department of Immunology and Serology, School of Pharmacy with the Division of Medical Analytics in Sosnowiec, Medical University of Silesia in Katowice, Jedności 8, 41-200, Sosnowiec, Poland. sikoraj@poczta.onet.pl.

Insights

Endometriosis is linked to higher levels of complement system proteins C1q, mannose-binding lectin (MBL), and C1 inhibitor (C1INH) in peritoneal fluid. These elevated levels may impair the clearance of ectopic endometrial cells and increase inflammation.

Area of Science:

  • Immunology
  • Reproductive Medicine
  • Complement System Biology

Background:

  • Endometriosis is a complex gynecological condition characterized by the presence of endometrial-like tissue outside the uterus.
  • The pathogenesis of endometriosis involves inflammation, immune dysregulation, and potential issues with the clearance of shed endometrial cells.
  • The complement system, a crucial part of innate immunity, plays a role in inflammation and cellular homeostasis.

Purpose of the Study:

  • To investigate the association between complement components C1q, mannose-binding lectin (MBL), and C1 inhibitor (C1INH) and the pathogenesis of endometriosis.
  • To determine if altered levels of these complement proteins in peritoneal fluid correlate with the presence or stage of endometriosis.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was employed to quantify concentrations of C1q, MBL, and C1INH.
  • Peritoneal fluid samples were collected from 80 women, including those with and without endometriosis.
  • Statistical analysis was performed to compare protein levels between groups and disease stages.

Main Results:

  • Significantly elevated levels of C1q, MBL, and C1INH were detected in the peritoneal fluid of women with endometriosis compared to controls (p < 0.0001).
  • Higher concentrations of these complement components were observed in women with early-stage endometriosis compared to those with advanced disease (p < 0.0001).

Conclusions:

  • The findings suggest dysregulation of the classical and lectin pathways of the complement system in the peritoneal cavity of endometriosis patients.
  • These abnormalities may contribute to impaired clearance of ectopic endometrial cells and enhanced local inflammation, key features of endometriosis pathogenesis.
Abstract

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