Cargando…

Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome

BACKGROUND: Acne is a chronic facial disease caused by Propionibacterium acnes, which proliferates within sebum-blocked skin follicles and increases inflammatory cytokine production. Several therapeutic drugs and products have been proposed to treat acne, yet no single treatment that ensures long-te...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Xiaoxi, Luo, Sai, Chen, Xinyao, Li, Shasha, Hao, Lijun, Yang, Dan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9308350/
https://www.ncbi.nlm.nih.gov/pubmed/35871079
http://dx.doi.org/10.1186/s13287-022-03007-7
_version_ 1784752966252625920
author Li, Xiaoxi
Luo, Sai
Chen, Xinyao
Li, Shasha
Hao, Lijun
Yang, Dan
author_facet Li, Xiaoxi
Luo, Sai
Chen, Xinyao
Li, Shasha
Hao, Lijun
Yang, Dan
author_sort Li, Xiaoxi
collection PubMed
description BACKGROUND: Acne is a chronic facial disease caused by Propionibacterium acnes, which proliferates within sebum-blocked skin follicles and increases inflammatory cytokine production. Several therapeutic drugs and products have been proposed to treat acne, yet no single treatment that ensures long-term treatment efficacy for all patients is available. Here, we explored the use of facial autologous fat transplant of adipose-derived stem cells (ADSCs) to dramatically reduce acne lesions. METHODS: THP-1 cells were treated with active P. acnes for 24 h at different multiplicities of infection, and alterations in inflammatory factors were detected. To study the effect of THP-1 on inflammasome-related proteins, we first co-cultured ADSCs with THP-1 cells treated with P. acnes and evaluated the levels of these proteins in the supernatant. Further, an acne mouse model injected with ADSCs was used to assess inflammatory changes. RESULTS: Propionibacterium acnes-mediated stimulation of THP-1 cells had a direct correlation with the expression of active caspase-1 and interleukin (IL)-1β in an infection-dependent manner. ADSCs significantly reduced the production of IL-1β induced by P. acnes stimulation through the reactive oxygen species (ROS)/Nod-like receptor family pyrin domain-containing 3 (NLRP3)/caspase-1 pathway. The results showed that ADSCs inhibit the skin inflammation induced by P. acnes by blocking the NLRP3 inflammasome via reducing the secretion of IL-1β in vivo. CONCLUSIONS: Our findings suggest that ADSCs can alter IL-1β secretion by restricting the production of mitochondria ROS, thereby inhibiting the NLRP3/caspase-1 pathway in P. acnes-induced inflammatory responses. This study indicates that anti‐acne therapy can potentially be developed by targeting the NLRP3 inflammasome. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13287-022-03007-7.
format Online
Article
Text
id pubmed-9308350
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-93083502022-07-24 Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome Li, Xiaoxi Luo, Sai Chen, Xinyao Li, Shasha Hao, Lijun Yang, Dan Stem Cell Res Ther Research BACKGROUND: Acne is a chronic facial disease caused by Propionibacterium acnes, which proliferates within sebum-blocked skin follicles and increases inflammatory cytokine production. Several therapeutic drugs and products have been proposed to treat acne, yet no single treatment that ensures long-term treatment efficacy for all patients is available. Here, we explored the use of facial autologous fat transplant of adipose-derived stem cells (ADSCs) to dramatically reduce acne lesions. METHODS: THP-1 cells were treated with active P. acnes for 24 h at different multiplicities of infection, and alterations in inflammatory factors were detected. To study the effect of THP-1 on inflammasome-related proteins, we first co-cultured ADSCs with THP-1 cells treated with P. acnes and evaluated the levels of these proteins in the supernatant. Further, an acne mouse model injected with ADSCs was used to assess inflammatory changes. RESULTS: Propionibacterium acnes-mediated stimulation of THP-1 cells had a direct correlation with the expression of active caspase-1 and interleukin (IL)-1β in an infection-dependent manner. ADSCs significantly reduced the production of IL-1β induced by P. acnes stimulation through the reactive oxygen species (ROS)/Nod-like receptor family pyrin domain-containing 3 (NLRP3)/caspase-1 pathway. The results showed that ADSCs inhibit the skin inflammation induced by P. acnes by blocking the NLRP3 inflammasome via reducing the secretion of IL-1β in vivo. CONCLUSIONS: Our findings suggest that ADSCs can alter IL-1β secretion by restricting the production of mitochondria ROS, thereby inhibiting the NLRP3/caspase-1 pathway in P. acnes-induced inflammatory responses. This study indicates that anti‐acne therapy can potentially be developed by targeting the NLRP3 inflammasome. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13287-022-03007-7. BioMed Central 2022-07-23 /pmc/articles/PMC9308350/ /pubmed/35871079 http://dx.doi.org/10.1186/s13287-022-03007-7 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Li, Xiaoxi
Luo, Sai
Chen, Xinyao
Li, Shasha
Hao, Lijun
Yang, Dan
Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome
title Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome
title_full Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome
title_fullStr Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome
title_full_unstemmed Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome
title_short Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome
title_sort adipose-derived stem cells attenuate acne-related inflammation via suppression of nlrp3 inflammasome
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9308350/
https://www.ncbi.nlm.nih.gov/pubmed/35871079
http://dx.doi.org/10.1186/s13287-022-03007-7
work_keys_str_mv AT lixiaoxi adiposederivedstemcellsattenuateacnerelatedinflammationviasuppressionofnlrp3inflammasome
AT luosai adiposederivedstemcellsattenuateacnerelatedinflammationviasuppressionofnlrp3inflammasome
AT chenxinyao adiposederivedstemcellsattenuateacnerelatedinflammationviasuppressionofnlrp3inflammasome
AT lishasha adiposederivedstemcellsattenuateacnerelatedinflammationviasuppressionofnlrp3inflammasome
AT haolijun adiposederivedstemcellsattenuateacnerelatedinflammationviasuppressionofnlrp3inflammasome
AT yangdan adiposederivedstemcellsattenuateacnerelatedinflammationviasuppressionofnlrp3inflammasome