Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage
- Li Xiao
- Wan-Hua Zhang
- Yin Huang
- Peng Huang
Affiliations: Department of Pediatrics, South Medical University Affiliated Maternal and Child Health Hospital of Foshan, Foshan, Guangdong 528000, P.R. China
- Published online on: December 17, 2021 https://doi.org/10.3892/etm.2021.11081
Copyright: © Xiao
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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.