Skip to main content
Erschienen in: Inflammation Research 4/2023

06.03.2023 | Original Research Paper

Amnion-derived serum amyloid A1 participates in sterile inflammation of fetal membranes at parturition

verfasst von: Yi-kai Lin, Fan Zhang, Wen-jia Lei, Xiao-wen Gan, Meng-die Li, Fan Pan, Wang-sheng Wang, Kang Sun

Erschienen in: Inflammation Research | Ausgabe 4/2023

Einloggen, um Zugang zu erhalten

Abstract

Objectives

Sterile inflammation of fetal membranes is an indispensable event of normal parturition. However, triggers of sterile inflammation are not fully resolved. Serum amyloid A1 (SAA1) is an acute phase protein produced primarily by the liver. Fetal membranes can also synthesize SAA1 but its functions are not well defined. Given the role of SAA1 in the acute phase response to inflammation, we postulated that SAA1 synthesized in the fetal membranes may be a trigger of local inflammation at parturition.

Methods

The changes of SAA1 abundance in parturition were studied in the amnion of human fetal membranes. The role of SAA1 in chemokine expression and leukocyte chemotaxis was examined in cultured human amnion tissue explants as well as primary human amnion fibroblasts. The effects of SAA1 on monocytes, macrophages and dendritic cells were investigated in cells derived from a human leukemia monocytic cell line (THP-1).

Results

SAA1 synthesis increased significantly in human amnion at parturition. SAA1 evoked multiple chemotaxis pathways in human amnion fibroblasts along with upregulation of a series of chemokines via both toll-like receptor 4 (TLR4) and formyl peptide receptor 2 (FPR2). Moreover, SAA1-conditioned medium of cultured amnion fibroblasts was capable of chemoattracting virtually all types of mononuclear leukocytes, particularly monocytes and dendritic cells, which reconciled with the chemotactic activity of conditioned medium of cultured amnion tissue explants collected from spontaneous labor. Furthermore, SAA1 could induce the expression of genes associated with inflammation and extracellular matrix remodeling in monocytes, macrophages and dendritic cells derived from THP-1.

Conclusions

SAA1 is a trigger of sterile inflammation of the fetal membranes at parturition.
Anhänge
Nur mit Berechtigung zugänglich
Literatur
4.
Zurück zum Zitat Bukowski R, Sadovsky Y, Goodarzi H, Zhang H, Biggio JR, Varner M, et al. Onset of human preterm and term birth is related to unique inflammatory transcriptome profiles at the maternal fetal interface. PeerJ. 2017;5:e3685.https://doi.org/10.7717/peerj.3685 Bukowski R, Sadovsky Y, Goodarzi H, Zhang H, Biggio JR, Varner M, et al. Onset of human preterm and term birth is related to unique inflammatory transcriptome profiles at the maternal fetal interface. PeerJ. 2017;5:e3685.https://​doi.​org/​10.​7717/​peerj.​3685
8.
Zurück zum Zitat Blencowe H, Cousens S, Oestergaard MZ, Chou D, Moller A-B, Narwal R, et al. National, regional, and worldwide estimates of preterm birth rates in the year 2010 with time trends since 1990 for selected countries: a systematic analysis and implications. The Lancet. 2012;379(9832):2162–72. https://doi.org/10.1016/s0140-6736(12)60820-4.CrossRef Blencowe H, Cousens S, Oestergaard MZ, Chou D, Moller A-B, Narwal R, et al. National, regional, and worldwide estimates of preterm birth rates in the year 2010 with time trends since 1990 for selected countries: a systematic analysis and implications. The Lancet. 2012;379(9832):2162–72. https://​doi.​org/​10.​1016/​s0140-6736(12)60820-4.CrossRef
12.
Zurück zum Zitat Menon R, Nicolau NN, Bredson S, Polettini J. Fetal membranes: Potential Source of Preterm Birth Biomarkers. General Methods in Biomarker Research and their Applications 2014. p. 1–35 Menon R, Nicolau NN, Bredson S, Polettini J. Fetal membranes: Potential Source of Preterm Birth Biomarkers. General Methods in Biomarker Research and their Applications 2014. p. 1–35
39.
Zurück zum Zitat Wang YW, Wang WS, Wang LY, Bao YR, Lu JW, Lu Y, et al. Extracellular matrix remodeling effects of serum amyloid A1 in the human amnion: Implications for fetal membrane rupture. Am J Reprod Immunol. 2019;81(1):e13073.https://doi.org/10.1111/aji.13073 Wang YW, Wang WS, Wang LY, Bao YR, Lu JW, Lu Y, et al. Extracellular matrix remodeling effects of serum amyloid A1 in the human amnion: Implications for fetal membrane rupture. Am J Reprod Immunol. 2019;81(1):e13073.https://​doi.​org/​10.​1111/​aji.​13073
44.
Zurück zum Zitat Houser BL. Decidual macrophages and their roles at the maternal-fetal interface. Yale J Biol Med. 2012;85(1):105–18.PubMedPubMedCentral Houser BL. Decidual macrophages and their roles at the maternal-fetal interface. Yale J Biol Med. 2012;85(1):105–18.PubMedPubMedCentral
53.
54.
Zurück zum Zitat Badolato R, Johnston JA, Wang JM, McVicar D, Xu LL, Oppenheim JJ, et al. Serum amyloid A induces calcium mobilization and chemotaxis of human monocytes by activating a pertussis toxin-sensitive signaling pathway. J Immunol. 1995;155(8):4004–10.CrossRefPubMed Badolato R, Johnston JA, Wang JM, McVicar D, Xu LL, Oppenheim JJ, et al. Serum amyloid A induces calcium mobilization and chemotaxis of human monocytes by activating a pertussis toxin-sensitive signaling pathway. J Immunol. 1995;155(8):4004–10.CrossRefPubMed
55.
Zurück zum Zitat Xu L, Badolato R, Murphy WJ, Longo DL, Anver M, Hale S, et al. A novel biologic function of serum amyloid A. Induction of T lymphocyte migration and adhesion. J Immunol. 1995;155(3):1184–90.CrossRefPubMed Xu L, Badolato R, Murphy WJ, Longo DL, Anver M, Hale S, et al. A novel biologic function of serum amyloid A. Induction of T lymphocyte migration and adhesion. J Immunol. 1995;155(3):1184–90.CrossRefPubMed
63.
Zurück zum Zitat Chanput W, Peters V, Wichers H. THP-1 and U937 Cells. In: Verhoeckx K, Cotter P, López-Expósito I, Kleiveland C, Lea T, Mackie A, et al., eds. The Impact of Food Bioactives on Health: in vitro and ex vivo models. Cham (CH): Springer, Copyright 2015, The Author(s). 2015. p. 147–59 Chanput W, Peters V, Wichers H. THP-1 and U937 Cells. In: Verhoeckx K, Cotter P, López-Expósito I, Kleiveland C, Lea T, Mackie A, et al., eds. The Impact of Food Bioactives on Health: in vitro and ex vivo models. Cham (CH): Springer, Copyright 2015, The Author(s). 2015. p. 147–59
Metadaten
Titel
Amnion-derived serum amyloid A1 participates in sterile inflammation of fetal membranes at parturition
verfasst von
Yi-kai Lin
Fan Zhang
Wen-jia Lei
Xiao-wen Gan
Meng-die Li
Fan Pan
Wang-sheng Wang
Kang Sun
Publikationsdatum
06.03.2023
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 4/2023
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-023-01713-3

Weitere Artikel der Ausgabe 4/2023

Inflammation Research 4/2023 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Bei Herzinsuffizienz muss „Eisenmangel“ neu definiert werden!

16.05.2024 Herzinsuffizienz Nachrichten

Bei chronischer Herzinsuffizienz macht es einem internationalen Expertenteam zufolge wenig Sinn, die Diagnose „Eisenmangel“ am Serumferritin festzumachen. Das Team schlägt vor, sich lieber an die Transferrinsättigung zu halten.

Herzinfarkt mit 85 – trotzdem noch intensive Lipidsenkung?

16.05.2024 Hypercholesterinämie Nachrichten

Profitieren nach einem akuten Myokardinfarkt auch Betroffene über 80 Jahre noch von einer intensiven Lipidsenkung zur Sekundärprävention? Um diese Frage zu beantworten, wurden jetzt Registerdaten aus Frankreich ausgewertet.

ADHS-Medikation erhöht das kardiovaskuläre Risiko

16.05.2024 Herzinsuffizienz Nachrichten

Erwachsene, die Medikamente gegen das Aufmerksamkeitsdefizit-Hyperaktivitätssyndrom einnehmen, laufen offenbar erhöhte Gefahr, an Herzschwäche zu erkranken oder einen Schlaganfall zu erleiden. Es scheint eine Dosis-Wirkungs-Beziehung zu bestehen.

Erstmanifestation eines Diabetes-Typ-1 bei Kindern: Ein Notfall!

16.05.2024 DDG-Jahrestagung 2024 Kongressbericht

Manifestiert sich ein Typ-1-Diabetes bei Kindern, ist das ein Notfall – ebenso wie eine diabetische Ketoazidose. Die Grundsäulen der Therapie bestehen aus Rehydratation, Insulin und Kaliumgabe. Insulin ist das Medikament der Wahl zur Behandlung der Ketoazidose.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.