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Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis

Background: Pyroptosis is a catabolic process relevant to periodontal disorders for which interleukin-1β (IL-1β) inflammation is central to the pathophysiology of the disease. Despite platelet-rich fibrin (PRF) anti-inflammatory properties and its application to support periodontal regeneration, the...

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Autores principales: Sordi, Mariane Beatriz, Panahipour, Layla, Kargarpour, Zahra, Gruber, Reinhard
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9368224/
https://www.ncbi.nlm.nih.gov/pubmed/35955441
http://dx.doi.org/10.3390/ijms23158306
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author Sordi, Mariane Beatriz
Panahipour, Layla
Kargarpour, Zahra
Gruber, Reinhard
author_facet Sordi, Mariane Beatriz
Panahipour, Layla
Kargarpour, Zahra
Gruber, Reinhard
author_sort Sordi, Mariane Beatriz
collection PubMed
description Background: Pyroptosis is a catabolic process relevant to periodontal disorders for which interleukin-1β (IL-1β) inflammation is central to the pathophysiology of the disease. Despite platelet-rich fibrin (PRF) anti-inflammatory properties and its application to support periodontal regeneration, the capacity of PRF to modulate pyroptosis, specifically the production and release of IL-1β, remains unknown. The question arises whether PRF could regulate IL-1β release from macrophages in vitro. Methods: To answer this question, RAW 264.7 macrophages and primary macrophages obtained from murine bone marrow were primed with PRF before being challenged by lipopolysaccharide (LPS). Cells were then analysed for the pyroptosis signalling components by gene expression analyses and IL-1β secretion at the protein level. The release of mitochondrial reactive oxygen species (ROS) was also detected. Results: PRF lowered the LPS-induced expression of IL-1β and NLRP3 inflammasome, caspase-11 and IL-18 in primary macrophages, and IL-1β and caspase-11 in RAW 264.7 cells. Additionally, PRF diminished the secretion of IL-1β at the protein level in LPS-induced RAW 264.7 cells. This was shown through immunoassays performed with the supernatant and further confirmed by analysing the lysates of permeabilised cells. Furthermore, PRF reduced the ROS release provoked by LPS in RAW 264.7 cells. Finally, to enhance IL-1β release from the LPS-primed macrophages, we introduced a second signal with adenosine triphosphate (ATP). In this setting, PRF significantly reduced IL-1β release in RAW 264.7 cells and a trend to diminish IL-1β release in primary macrophages. Conclusion: These findings suggest that PRF can reduce IL-1β release and, at least in part, inhibit pyroptosis-related factors in LPS-challenged macrophages.
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spelling pubmed-93682242022-08-12 Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis Sordi, Mariane Beatriz Panahipour, Layla Kargarpour, Zahra Gruber, Reinhard Int J Mol Sci Article Background: Pyroptosis is a catabolic process relevant to periodontal disorders for which interleukin-1β (IL-1β) inflammation is central to the pathophysiology of the disease. Despite platelet-rich fibrin (PRF) anti-inflammatory properties and its application to support periodontal regeneration, the capacity of PRF to modulate pyroptosis, specifically the production and release of IL-1β, remains unknown. The question arises whether PRF could regulate IL-1β release from macrophages in vitro. Methods: To answer this question, RAW 264.7 macrophages and primary macrophages obtained from murine bone marrow were primed with PRF before being challenged by lipopolysaccharide (LPS). Cells were then analysed for the pyroptosis signalling components by gene expression analyses and IL-1β secretion at the protein level. The release of mitochondrial reactive oxygen species (ROS) was also detected. Results: PRF lowered the LPS-induced expression of IL-1β and NLRP3 inflammasome, caspase-11 and IL-18 in primary macrophages, and IL-1β and caspase-11 in RAW 264.7 cells. Additionally, PRF diminished the secretion of IL-1β at the protein level in LPS-induced RAW 264.7 cells. This was shown through immunoassays performed with the supernatant and further confirmed by analysing the lysates of permeabilised cells. Furthermore, PRF reduced the ROS release provoked by LPS in RAW 264.7 cells. Finally, to enhance IL-1β release from the LPS-primed macrophages, we introduced a second signal with adenosine triphosphate (ATP). In this setting, PRF significantly reduced IL-1β release in RAW 264.7 cells and a trend to diminish IL-1β release in primary macrophages. Conclusion: These findings suggest that PRF can reduce IL-1β release and, at least in part, inhibit pyroptosis-related factors in LPS-challenged macrophages. MDPI 2022-07-27 /pmc/articles/PMC9368224/ /pubmed/35955441 http://dx.doi.org/10.3390/ijms23158306 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Sordi, Mariane Beatriz
Panahipour, Layla
Kargarpour, Zahra
Gruber, Reinhard
Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis
title Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis
title_full Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis
title_fullStr Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis
title_full_unstemmed Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis
title_short Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis
title_sort platelet-rich fibrin reduces il-1β release from macrophages undergoing pyroptosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9368224/
https://www.ncbi.nlm.nih.gov/pubmed/35955441
http://dx.doi.org/10.3390/ijms23158306
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