Cargando…

Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage

Intestinal ischemia-reperfusion (I/R) injury promotes the release of IL-17A, and previous studies have indicated that TGF-β activated kinase 1 (TAK1) is an important signaling molecule in the regulatory function of IL-17A. The present study aimed to explore the potential effects of IL-17A release in...

Descripción completa

Detalles Bibliográficos
Autores principales: Xiao, Li, Zhang, Wan-Hua, Huang, Yin, Huang, Peng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8753980/
https://www.ncbi.nlm.nih.gov/pubmed/35069839
http://dx.doi.org/10.3892/etm.2021.11081
_version_ 1784632184227758080
author Xiao, Li
Zhang, Wan-Hua
Huang, Yin
Huang, Peng
author_facet Xiao, Li
Zhang, Wan-Hua
Huang, Yin
Huang, Peng
author_sort Xiao, Li
collection PubMed
description Intestinal ischemia-reperfusion (I/R) injury promotes the release of IL-17A, and previous studies have indicated that TGF-β activated kinase 1 (TAK1) is an important signaling molecule in the regulatory function of IL-17A. The present study aimed to explore the potential effects of IL-17A release in intestinal I/R injury, and to investigate the underlying regulatory mechanisms. Initially, the expression levels of TAK1 and JNK in a hypoxia/reoxygenation model were determined, and the effects of TAK1-knockdown on JNK phosphorylation and the viability, inflammation, apoptosis and barrier function of Caco-2 cells were assessed using Cell Counting Kit-8, reverse transcription-quantitative PCR, TUNEL and transepithelial electrical resistance assays, respectively. Subsequently, an antibody targeting IL-17A was used, and the effects of the IL-17A antibody on the expression levels of TAK1 as well as cell viability, inflammation, apoptosis and barrier function were determined. The results of the present study demonstrated that TAK1-knockdown markedly reduced JNK phosphorylation and improved the levels of cell viability, inflammation, apoptosis and barrier function via the MAPK signaling pathway. In addition, treatment with the IL-17A antibody inhibited the expression of TAK1, and reversed the aforementioned effects of TAK1 on Caco-2 cells. In conclusion, intestinal I/R induces the release of IL-17A to regulate cell viability, inflammation, apoptosis and barrier damage via the TAK1/MAPK signaling pathway.
format Online
Article
Text
id pubmed-8753980
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher D.A. Spandidos
record_format MEDLINE/PubMed
spelling pubmed-87539802022-01-21 Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage Xiao, Li Zhang, Wan-Hua Huang, Yin Huang, Peng Exp Ther Med Articles Intestinal ischemia-reperfusion (I/R) injury promotes the release of IL-17A, and previous studies have indicated that TGF-β activated kinase 1 (TAK1) is an important signaling molecule in the regulatory function of IL-17A. The present study aimed to explore the potential effects of IL-17A release in intestinal I/R injury, and to investigate the underlying regulatory mechanisms. Initially, the expression levels of TAK1 and JNK in a hypoxia/reoxygenation model were determined, and the effects of TAK1-knockdown on JNK phosphorylation and the viability, inflammation, apoptosis and barrier function of Caco-2 cells were assessed using Cell Counting Kit-8, reverse transcription-quantitative PCR, TUNEL and transepithelial electrical resistance assays, respectively. Subsequently, an antibody targeting IL-17A was used, and the effects of the IL-17A antibody on the expression levels of TAK1 as well as cell viability, inflammation, apoptosis and barrier function were determined. The results of the present study demonstrated that TAK1-knockdown markedly reduced JNK phosphorylation and improved the levels of cell viability, inflammation, apoptosis and barrier function via the MAPK signaling pathway. In addition, treatment with the IL-17A antibody inhibited the expression of TAK1, and reversed the aforementioned effects of TAK1 on Caco-2 cells. In conclusion, intestinal I/R induces the release of IL-17A to regulate cell viability, inflammation, apoptosis and barrier damage via the TAK1/MAPK signaling pathway. D.A. Spandidos 2022-02 2021-12-17 /pmc/articles/PMC8753980/ /pubmed/35069839 http://dx.doi.org/10.3892/etm.2021.11081 Text en Copyright: © Xiao et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Xiao, Li
Zhang, Wan-Hua
Huang, Yin
Huang, Peng
Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage
title Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage
title_full Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage
title_fullStr Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage
title_full_unstemmed Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage
title_short Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage
title_sort intestinal ischemia-reperfusion induces the release of il-17a to regulate cell inflammation, apoptosis and barrier damage
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8753980/
https://www.ncbi.nlm.nih.gov/pubmed/35069839
http://dx.doi.org/10.3892/etm.2021.11081
work_keys_str_mv AT xiaoli intestinalischemiareperfusioninducesthereleaseofil17atoregulatecellinflammationapoptosisandbarrierdamage
AT zhangwanhua intestinalischemiareperfusioninducesthereleaseofil17atoregulatecellinflammationapoptosisandbarrierdamage
AT huangyin intestinalischemiareperfusioninducesthereleaseofil17atoregulatecellinflammationapoptosisandbarrierdamage
AT huangpeng intestinalischemiareperfusioninducesthereleaseofil17atoregulatecellinflammationapoptosisandbarrierdamage