Interleukin-1 beta is significantly upregulated in the decidua of spontaneous and recurrent miscarriage placentas.
First trimester placenta
Interleukin-1 beta
Recurrent miscarriage
Spontaneous miscarriage
Journal
Journal of reproductive immunology
ISSN: 1872-7603
Titre abrégé: J Reprod Immunol
Pays: Ireland
ID NLM: 8001906
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
18
09
2020
revised:
07
01
2021
accepted:
26
01
2021
pubmed:
6
2
2021
medline:
6
11
2021
entrez:
5
2
2021
Statut:
ppublish
Résumé
Pregnancy is an extraordinarily complex immunological process. For successful pregnancy maintenance the maternal immune system must adapt to and tolerate the semi-allogenic fetus at the fetomaternal interface of the placenta. This balance is regulated by cytokines with a predominant T helper 2 (Th-2) system and a suppressed inflammatory T helper 1 (Th-1) response. This study investigates the role of the Th-1 pro-inflammatory cytokine Interleukin-1 beta (IL-1β) and its role in early pregnancy loss. In order to identify differences in IL- β levels a TaqMan® Human Cytokine Network Array, with placental tissue obtained from patients with healthy pregnancies (n = 15) and recurrent miscarriage (n = 15), was carried out. Protein expression of IL-1β in the decidua of healthy pregnancies (n = 15), spontaneous (n = 18) and recurrent miscarriages (n = 15), was investigated by immunohistochemistry. The identification of IL-1β expressing cells in the decidua was done with double-immunofluorescence. Gene expression analysis identified a nearly 54-times higher expression of IL-1β in placental tissue of patients suffering from recurrent abortion. Immunohistochemistry confirmed a significant upregulation of IL-1β in the decidua of recurrent miscarriage specimens (p = 0.01) as well as in the decidua of women with spontaneous abortion (p = 0.001). Double-immunofluorescence identified decidual stoma cells as IL-1β expressing cells. Significant upregulation of IL-1β may be associated with an imbalanced immune system and a procoagulant state that could be responsible for early pregnancy loss. These results provide new evidence of the complex interplay of IL-1β at the fetomaternal interface and its crucial role in miscarriage processes.
Sections du résumé
BACKGROUND
Pregnancy is an extraordinarily complex immunological process. For successful pregnancy maintenance the maternal immune system must adapt to and tolerate the semi-allogenic fetus at the fetomaternal interface of the placenta. This balance is regulated by cytokines with a predominant T helper 2 (Th-2) system and a suppressed inflammatory T helper 1 (Th-1) response. This study investigates the role of the Th-1 pro-inflammatory cytokine Interleukin-1 beta (IL-1β) and its role in early pregnancy loss.
PATIENTS AND METHODS
In order to identify differences in IL- β levels a TaqMan® Human Cytokine Network Array, with placental tissue obtained from patients with healthy pregnancies (n = 15) and recurrent miscarriage (n = 15), was carried out. Protein expression of IL-1β in the decidua of healthy pregnancies (n = 15), spontaneous (n = 18) and recurrent miscarriages (n = 15), was investigated by immunohistochemistry. The identification of IL-1β expressing cells in the decidua was done with double-immunofluorescence.
RESULTS
Gene expression analysis identified a nearly 54-times higher expression of IL-1β in placental tissue of patients suffering from recurrent abortion. Immunohistochemistry confirmed a significant upregulation of IL-1β in the decidua of recurrent miscarriage specimens (p = 0.01) as well as in the decidua of women with spontaneous abortion (p = 0.001). Double-immunofluorescence identified decidual stoma cells as IL-1β expressing cells.
CONCLUSION
Significant upregulation of IL-1β may be associated with an imbalanced immune system and a procoagulant state that could be responsible for early pregnancy loss. These results provide new evidence of the complex interplay of IL-1β at the fetomaternal interface and its crucial role in miscarriage processes.
Identifiants
pubmed: 33545613
pii: S0165-0378(21)00013-9
doi: 10.1016/j.jri.2021.103283
pii:
doi:
Substances chimiques
IL1B protein, human
0
Interleukin-1beta
0
Types de publication
Journal Article
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
103283Informations de copyright
Copyright © 2021 Elsevier B.V. All rights reserved.