Deoxynivalenol Induces Inflammation in IPEC-J2 Cells by Activating P38 Mapk And Erk1/2
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
31572576
National Natural Science Foundation of China - International
2016T90477
China Postdoctoral Science Foundation - International
2016YFD0501207, 2016YFD0501009
National Key R & D Program - International
PubMed
32183221
PubMed Central
PMC7150952
DOI
10.3390/toxins12030180
PII: toxins12030180
Knihovny.cz E-zdroje
- Klíčová slova
- IPEC-J2 cells, MAPKs, RNA-seq, deoxynivalenol, inflammation,
- MeSH
- buněčné linie MeSH
- epitelové buňky účinky léků imunologie metabolismus MeSH
- interleukin-1 genetika MeSH
- interleukin-6 genetika MeSH
- MAP kinasový signální systém účinky léků genetika imunologie MeSH
- mitogenem aktivované proteinkinasy p38 metabolismus MeSH
- prasata MeSH
- střevní sliznice účinky léků imunologie metabolismus MeSH
- TNF-alfa genetika MeSH
- transkriptom účinky léků MeSH
- trichotheceny toxicita MeSH
- viabilita buněk účinky léků MeSH
- zánět MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- deoxynivalenol MeSH Prohlížeč
- interleukin-1 MeSH
- interleukin-6 MeSH
- mitogenem aktivované proteinkinasy p38 MeSH
- TNF-alfa MeSH
- trichotheceny MeSH
Fusarium-derived mycotoxin deoxynivalenol (DON) usually induces diarrhea, vomiting and gastrointestinal inflammation. We studied the cytotoxic effect of DON on porcine small intestinal epithelium using the intestinal porcine epithelial cell line IPEC-J2. We screened out differentially expressed genes (DEGs) using RNA-seq and identified 320 upregulated genes and 160 downregulated genes. The enrichment pathways of these DEGs focused on immune-related pathways. DON induced proinflammatory gene expression, including cytokines, chemokines and other inflammation-related genes. DON increased IL1A, IL6 and TNF-α release and DON activated the phosphorylation of extracellular signal-regulated kinase-1 and-2 (ERK1/2), JUN N-terminal kinase (JNK) and p38 MAPK. A p38 inhibitor attenuated DON-induced IL6, TNF-α, CXCL2, CXCL8, IL12A, IL1A, CCL20, CCL4 and IL15 production, while an ERK1/2 inhibitor had only a small inhibitory effect on IL15 and IL6. An inhibitor of p38 MAPK decreased the release of IL1A, IL6 and TNF-α and an inhibitor of ERK1/2 partly attenuated protein levels of IL6. These data demonstrate that DON induces proinflammatory factor production in IPEC-J2 cells by activating p38 and ERK1/2.
College of Veterinary Medicine Nanjing Agricultural University Nanjing 210095 China
Jiangsu Vocational College of Agriculture and Forestry Jurong 212400 China
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