AI Article Synopsis

  • The gut is the primary pathway for mycotoxin exposure, such as zearalenone (ZEA), which raises concerns about its effects on intestinal cells.
  • Treatment of porcine epithelial cells with 10μM ZEA for 24 hours revealed no negative impact on cell viability but did trigger an increase in various inflammatory cytokines and toll-like receptors.
  • The microarray analysis highlighted significant gene expression changes, with 190 genes affected, including up-regulation of genes important for immune response, mucosal protection, and potential carcinogenic effects.

Article Abstract

The gut represents the main route of intoxication with mycotoxins. To evaluate the effect and the underlying molecular changes that occurred when the intestine is exposed to zearalenone, a Fusarium sp mycotoxin, porcine epithelial cells (IPEC-1) were treated with 10μM of ZEA for 24h and analysed by microarray using Gene Spring GX v.11.5. Our results showed that 10μM of ZEA did not affect cell viability, but can increase the expression of toll like receptors (TLR1-10) and of certain cytokines involved in inflammation (TNF-α, IL-1β, IL-6, IL-8, MCP-1, IL-12p40, CCL20) or responsible for the recruitment of immune cells (IL-10, IL-18). Microarray results identified 190 genes significantly and differentially expressed, of which 70% were up-regulated. ZEA determined the over expression of ITGB5 gene, essential against the attachment and adhesion of ETEC to porcine jejunal cells and of TFF2 implicated in mucosal protection. An up-regulation of glutathione peroxidase enzymes (GPx6, GPx2, GPx1) was also observed. Upon ZEA challenge, genes like GTF3C4 responsible for the recruitment of polymerase III and initiation of tRNA transcription in eukaryotes and STAT5B were significantly higher induced. The up-regulation of CD97 gene and the down-regulation of tumour suppressor genes (DKK-1, PCDH11X and TC531386) demonstrates the carcinogenic potential of ZEA.

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Source
http://dx.doi.org/10.1016/j.toxlet.2014.10.022DOI Listing

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