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

  • Authors:
    • Li Xiao
    • Wan-Hua Zhang
    • Yin Huang
    • Peng Huang
  • View Affiliations / Copyright

    Affiliations: Department of Pediatrics, South Medical University Affiliated Maternal and Child Health Hospital of Foshan, Foshan, Guangdong 528000, P.R. China
    Copyright: © Xiao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 158
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    Published online on: December 17, 2021
       https://doi.org/10.3892/etm.2021.11081
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Xiao L, Zhang W, Huang Y and Huang P: Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage. Exp Ther Med 23: 158, 2022.
APA
Xiao, L., Zhang, W., Huang, Y., & Huang, P. (2022). Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage. Experimental and Therapeutic Medicine, 23, 158. https://doi.org/10.3892/etm.2021.11081
MLA
Xiao, L., Zhang, W., Huang, Y., Huang, P."Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage". Experimental and Therapeutic Medicine 23.2 (2022): 158.
Chicago
Xiao, L., Zhang, W., Huang, Y., Huang, P."Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage". Experimental and Therapeutic Medicine 23, no. 2 (2022): 158. https://doi.org/10.3892/etm.2021.11081
Copy and paste a formatted citation
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Spandidos Publications style
Xiao L, Zhang W, Huang Y and Huang P: Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage. Exp Ther Med 23: 158, 2022.
APA
Xiao, L., Zhang, W., Huang, Y., & Huang, P. (2022). Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage. Experimental and Therapeutic Medicine, 23, 158. https://doi.org/10.3892/etm.2021.11081
MLA
Xiao, L., Zhang, W., Huang, Y., Huang, P."Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage". Experimental and Therapeutic Medicine 23.2 (2022): 158.
Chicago
Xiao, L., Zhang, W., Huang, Y., Huang, P."Intestinal ischemia‑reperfusion induces the release of IL‑17A to regulate cell inflammation, apoptosis and barrier damage". Experimental and Therapeutic Medicine 23, no. 2 (2022): 158. https://doi.org/10.3892/etm.2021.11081
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