Effects of Deoxynivalenol and Mycotoxin Adsorbent Agents on Mitogen-Activated Protein Kinase Signaling Pathways and Inflammation-Associated Gene Expression in Porcine Intestinal Epithelial Cells

Abstract

Deoxynivalenol (DON) is the most prevalent mycotoxin in swine feedstuffs. The intestinal epithelial cells represent the first target for the DON. Here, we studied the effects of DON and mycotoxin adsorbent agents on mitogen-activated protein kinase (MAPK) signaling pathways and inflammation-associated gene expression in porcine intestinal epithelial cells (IPEC-J2). Results showed that phosphorylation of MAPK signaling pathways (p38, ERK, and JNK) was increased after treatment of DON or lipopolysaccharide (LPS) in IPEC-J2 cells. The phosphorylation of p38, ERK, and JNK was not further enhanced after co-treatment with DON and LPS. The inos and cox-2 mRNA expression were significantly induced at 6 h after treatment of DON. DON treatment significantly increased the claudin 3 and occludin mRNA expression at 12 h. DON in combination with LPS treatment did not further increase the inflammation and tight junction-associated gene expression. The DON-induced phosphorylation of MAPK signaling pathways was impaired by mycotoxin adsorbent agent (nanoscale silicate platelets and the mixture of montmorillonites and yeast cell walls) treatment, thereby decreasing inflammation and tight junction-associated gene expression. Taken together, these findings demonstrate that DON triggers the inflammation in IPEC-J2 cells by phosphorylation of MAPK signaling pathways and LPS does not further augment the DON-induced inflammatory responses. Mycotoxin adsorbent agents can attenuate DON-induced inflammatory responses in IPEC-J2 cells through modulation of the phosphorylation of p38, ERK, and JNK.