Does the Use of the "Proseek® Multiplex Inflammation I Panel" Demonstrate a Difference in Local and Systemic Immune Responses in Endometriosis Patients with or without Deep-Infiltrating Lesions?

Alexandra Perricos; Heinrich Husslein; Lorenz Kuessel; Manuela Gstoettner; Andreas Weinhaeusel; Thomas Eiwegger; Gabriel Beikircher; René Wenzl

doi:10.3390/ijms24055022

Does the Use of the "Proseek^® Multiplex Inflammation I Panel" Demonstrate a Difference in Local and Systemic Immune Responses in Endometriosis Patients with or without Deep-Infiltrating Lesions?

Int J Mol Sci. 2023 Mar 6;24(5):5022. doi: 10.3390/ijms24055022.

Authors

Affiliations

¹ Department of Obstetrics and Gynecology, Medical University of Vienna, 1090 Vienna, Austria.
² Molecular Diagnostics, Center for Health & Bioresources, AIT Austrian Institute of Technology Vienna, 1210 Vienna, Austria.
³ Translational Medicine Program, Research Institute, The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada.
⁴ Departments of Pediatric, Temerty Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada.
⁵ Departments of Immunology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada.
⁶ Medical Faculty, Karl Landsteiner University of Health Sciences, 3500 Krems an der Donau, Austria.
⁷ Department of Pediatric and Adolescent Medicine, University Hospital St. Pölten, 3100 St. Pölten, Austria.

Abstract

Endometriotic lesions are able to infiltrate surrounding tissue. This is made possible partly by an altered local and systemic immune response that helps achieve neoangiogenesis, cell proliferation and immune escape. Deep-infiltrating endometriosis (DIE) differs from other subtypes through the invasion of its lesions over 5 mm into affected tissue. Despite the invasive nature of these lesions and the wider range of symptoms they can trigger, DIE is described as a stable disease. This elicits the need for a better understanding of the underlying pathogenesis. We used the "Proseek^® Multiplex Inflammation I Panel" in order to simultaneously detect 92 inflammatory proteins in plasma and peritoneal fluid (PF) of controls and patients with endometriosis, as well as in particular patients with DIE, in order to gain a better insight into the systemically and locally involved immune response. Extracellular newly identified receptor for advanced gycation end-products binding protein (EN-RAGE), C-C motif Chemokine ligand 23 (CCL23), Eukaryotic translation initiation factor 4-binding protein 1 (4E-BP1) and human glial cell-line derived neurotrophic factor (hGDNF) were significantly increased in plasma of endometriosis patients compared to controls, whereas Hepatocyte Growth factor (HGF) and TNF-related apoptosis inducing ligand (TRAIL) were decreased. In PF of endometriosis patients, we found Interleukin 18 (IL-18) to be decreased, yet Interleukin 8 (IL-8) and Interleukin 6 (IL-6) to be increased. TNF-related activation-induced cytokine (TRANCE) and C-C motif Chemokine ligand 11 (CCL11) were significantly decreased in plasma, whereas C-C motif Chemokine ligand 23 (CCL23), Stem Cell Factor (SCF) and C-X-C motif chemokine 5 (CXCL5) were significantly increased in PF of patients with DIE compared to endometriosis patients without DIE. Although DIE lesions are characterized by increased angiogenetic and pro-inflammatory properties, our current study seems to support the theory that the systemic immune system does not play a major role in the pathogenesis of these lesions.

Keywords: endometriosis; inflammation; multiplex analysis.

MeSH terms

Ascitic Fluid / metabolism
Endometriosis* / pathology
Female
Humans
Inflammation / metabolism
Interleukin-6 / metabolism
Ligands

Substances

Ligands
Interleukin-6

Grants and funding

This research received no external funding.