The intestinal epithelium performs vital functions such as nutrient absorption and acting as an intestinal barrier to maintain the host’s homeostasis. Mycotoxin, which affects the processing and storage of animal feedstuff, is a problematic pollutant in farming products. Ochratoxin A generated by Aspergillus and Penicillium fungi causes inflammation, intestinal dysfunction, decline in growth, and reduced intake in porcine and other livestock. Despite these ongoing problems, OTA-related studies in intestinal epithelium are lacking. This study aimed to demonstrate that OTA regulates TLR/MyD88 signaling in IPEC-J2 cells and induces barrier function impairment through tight junction reduction. We measured expression of TLR/MyD88 signaling-related mRNAs and proteins. The indicator of intestinal barrier integrity was confirmed through immunofluorescence and transepithelial electrical resistance. Additionally, we confirmed whether inflammatory cytokines and barrier function were affected by MyD88 inhibition. MyD88 inhibition alleviated inflammatory cytokine levels, tight junction reduction, and damage to barrier function due to OTA. These results indicate that OTA induces TLR/MyD88 signaling-related genes and impairs tight junctions and intestinal barrier function in IPEC-J2 cells. MyD88 regulation in OTA-treated IPEC-J2 cells mitigates the tight junction and intestinal barrier function impairments. Our findings provide a molecular understanding of OTA toxicity in porcine intestinal epithelial cells.

Journal of Animal Science and Technology (JAST) is a peer-reviewed, open access journal publishing original research, review articles and notes in all fields of animal science. Topics covered by the journal include: genetics and breeding, physiology, nutrition of monogastric animals, nutrition of ruminants, animal products (milk, meat, eggs and their by-products) and their processing, grasslands and roughages, livestock environment, animal biotechnology, animal behavior and welfare.

Antimicrobial peptides (AMPs) function to extensively suppress various problematic factors and are considered a new alternative for improving livestock health and enhancing immunomodulation. In this study, we explored whether AMP regulation has positive influences on Ochratoxin A (OTA) exposure using a porcine intestinal epithelial cell line (IPEC-J2 cells). We constructed a beta-defensin 1 (DEFB1) expression vector and used it to transfection IPEC-J2 cells to construct AMP overexpression cell lines. The results showed that OTA induced cytotoxicity, decreased cell migration, and increased inflammatory markers mRNA in IPEC-J2 cells. In DEFB1 overexpressing cell lines, OTA-induced reduced cell migration and increased inflammatory markers mRNA were alleviated. Additionally, a natural product capable of inducing DEFB1 expression, which was selected through high-throughput screening, showed significant alleviation of cytotoxicity, cell migration, and inflammatory markers compared to OTA-treated IPEC-J2 cells. Our finding provides novel insights and clues for the porcine industry, which is affected by OTA exposure.

Background/Objectives: Intestinal dysfunction during weaning in piglets causes declines in growth through hindered absorption capacity and intestinal barrier function, equating to economic losses for the porcine industry. Established strategies for mitigating these negative issues are currently lacking. Methods: We evaluated biomolecular alterations induced by weaning stress through gene expression profiling and metabolome analysis using intestinal samples collected from piglets before weaning, 1 week after weaning, and 2 weeks after weaning. Results: We identified 701 differentially expressed genes related to weaning stress, representing the enrichment of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with immune response; inflammatory response; cell proliferation; cell adhesion; and carbohydrate, lipid, and calcium ion binding. In the metabolome analysis, ABC transporter; purine, pyrimidine, and Gly-Ser-Thr metabolisms; and the urea cycle were clustered as enriched KEGG pathways. Our results suggest that energy metabolism, including protein metabolism, is involved in the repair of the structural damage occurring in the intestine during weaning. Conclusions: This study highlights the importance of integrated analyses synthesizing molecular and metabolic mechanisms in elucidating complex biological responses and provides insights into markers that can be used to develop strategies for mitigating weaning stress in the porcine industry.

Fumonisin B1 (FB1) is a mycotoxin commonly found in animal feed, particularly in corn-based products. Exposure to FB1 can damage multiple organs, including the intestine, but its molecular effects on intestinal epithelial cells remain incompletely understood. This study investigated FB1-induced toxicity in porcine intestinal epithelial (IPEC-J2) cells and screened natural products for protective effects. Exploratory gene expression profiling identified genes showing predefined expression changes following FB1 exposure, and subsequent Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated associations with apoptosis-related processes. Annexin V/propidium iodide staining showed increased apoptosis-associated staining, while quantitative real-time polymerase chain reaction (qRT-PCR) showed altered expression of BCL2, CASP3, and CASP9. To identify protective candidates, 332 natural products were evaluated using high-throughput screening. Among the screened extracts, C. communis showed the highest cell viability in the primary screening and was selected for further investigation. Co-treatment with C. communis was associated with reduced apoptosis-associated staining and partial counteraction of FB1-associated changes in apoptosis-related gene expression. These findings suggest that C. communis warrants further investigation as a natural product for mitigating FB1-associated intestinal epithelial toxicity.