JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin
The most prevalent contaminated mycotoxin in feed and grain is T-2 toxin. The T-2 toxin's primary action target is the gut because it is the main organ of absorption. T-2 toxin can cause intestinal damage, but, few molecular mechanisms have been elucidated. It is important to discover the key p...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-09-01
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| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651323007510 |
| _version_ | 1797683205438963712 |
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| author | Fengjuan Chen Youshuang Wang Yunhe Chen Jiayan Fan Cong Zhang Xiuyuan He Xu Yang |
| author_facet | Fengjuan Chen Youshuang Wang Yunhe Chen Jiayan Fan Cong Zhang Xiuyuan He Xu Yang |
| author_sort | Fengjuan Chen |
| collection | DOAJ |
| description | The most prevalent contaminated mycotoxin in feed and grain is T-2 toxin. The T-2 toxin's primary action target is the gut because it is the main organ of absorption. T-2 toxin can cause intestinal damage, but, few molecular mechanisms have been elucidated. It is important to discover the key pathways by which T-2 toxin causes enterotoxicity. In this research, IPEC-J2 cells are used as a cell model to investigate the function of the MAPK signaling pathway in T-2 toxin-induced intestinal epithelial cell damage. Throughout this research, T-2 toxin results in functional impairment in IPEC-J2 cells by reducing the TJ proteins Claudin, Occludin-1, ZO-1, N-cadherin, and CX-43 expression. T-2 toxin significantly reduced the survival of IPEC-J2 cells and increased LDH release in a dose-dependent way. T-2 toxin induced IPEC-J2 cell oxidative stress by raising ROS and MDA content, and mitochondrial damage was indicated by a decline in MMP and an increase in the opening degree of MPTP. T-2 toxin upregulated the expression of ERK, P38 and JNK, which triggered the MAPK signaling pathway. In addition, T-2 toxin caused IPEC-J2 cell inflammation responses reflected by increased the levels of inflammation-related factors IL-8, p65, P-p65 and IL-6, and down-regulated IL-10 expression level. Inhibition JNK molecule can ease IPEC-J2 cell functional impairment and inflammatory response. In conclusion, as a consequence of the T-2 toxin activating the JNK molecule, oxidative stress and mitochondrial damage are induced, which impair cellular inflammation. |
| first_indexed | 2024-03-12T00:11:11Z |
| format | Article |
| id | doaj.art-7896c88a0c034ea98176984a0577f600 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-03-12T00:11:11Z |
| publishDate | 2023-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-7896c88a0c034ea98176984a0577f6002023-09-16T05:28:18ZengElsevierEcotoxicology and Environmental Safety0147-65132023-09-01263115247JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxinFengjuan Chen0Youshuang Wang1Yunhe Chen2Jiayan Fan3Cong Zhang4Xiuyuan He5Xu Yang6College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002 Henan, ChinaCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002 Henan, ChinaCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002 Henan, ChinaCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002 Henan, ChinaCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002 Henan, ChinaCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002 Henan, ChinaCorrespondence to: College of Veterinary Medicine, Henan Agricultural University, No.15 Longzihu University Park, Zhengdong New District, Zhengzhou 450046, China.; College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002 Henan, ChinaThe most prevalent contaminated mycotoxin in feed and grain is T-2 toxin. The T-2 toxin's primary action target is the gut because it is the main organ of absorption. T-2 toxin can cause intestinal damage, but, few molecular mechanisms have been elucidated. It is important to discover the key pathways by which T-2 toxin causes enterotoxicity. In this research, IPEC-J2 cells are used as a cell model to investigate the function of the MAPK signaling pathway in T-2 toxin-induced intestinal epithelial cell damage. Throughout this research, T-2 toxin results in functional impairment in IPEC-J2 cells by reducing the TJ proteins Claudin, Occludin-1, ZO-1, N-cadherin, and CX-43 expression. T-2 toxin significantly reduced the survival of IPEC-J2 cells and increased LDH release in a dose-dependent way. T-2 toxin induced IPEC-J2 cell oxidative stress by raising ROS and MDA content, and mitochondrial damage was indicated by a decline in MMP and an increase in the opening degree of MPTP. T-2 toxin upregulated the expression of ERK, P38 and JNK, which triggered the MAPK signaling pathway. In addition, T-2 toxin caused IPEC-J2 cell inflammation responses reflected by increased the levels of inflammation-related factors IL-8, p65, P-p65 and IL-6, and down-regulated IL-10 expression level. Inhibition JNK molecule can ease IPEC-J2 cell functional impairment and inflammatory response. In conclusion, as a consequence of the T-2 toxin activating the JNK molecule, oxidative stress and mitochondrial damage are induced, which impair cellular inflammation.http://www.sciencedirect.com/science/article/pii/S0147651323007510T-2 toxinJNKIntestinal epithelial cellsTight junctionInflammation |
| spellingShingle | Fengjuan Chen Youshuang Wang Yunhe Chen Jiayan Fan Cong Zhang Xiuyuan He Xu Yang JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin Ecotoxicology and Environmental Safety T-2 toxin JNK Intestinal epithelial cells Tight junction Inflammation |
| title | JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin |
| title_full | JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin |
| title_fullStr | JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin |
| title_full_unstemmed | JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin |
| title_short | JNK molecule is a toxic target for IPEC-J2 cell barrier damage induced by T-2 toxin |
| title_sort | jnk molecule is a toxic target for ipec j2 cell barrier damage induced by t 2 toxin |
| topic | T-2 toxin JNK Intestinal epithelial cells Tight junction Inflammation |
| url | http://www.sciencedirect.com/science/article/pii/S0147651323007510 |
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