Pyroptosis-Mediated Damage Mechanism by Deoxynivalenol in Porcine Small Intestinal Epithelial Cells.
Tae Hong KangSangsu ShinJeongWoong ParkBo-Ram LeeSang In LeePublished in: Toxins (2023)
Deoxynivalenol (DON) is known as a vomitoxin, which frequently contaminates feedstuffs, such as corn, wheat, and barley. Intake of DON-contaminated feed has been known to cause undesirable effects, including diarrhea, emesis, reduced feed intake, nutrient malabsorption, weight loss, and delay in growth, in livestock. However, the molecular mechanism of DON-induced damage of the intestinal epithelium requires further investigation. Treatment with DON triggered ROS in IPEC-J2 cells and increased the mRNA and protein expression levels of thioredoxin interacting protein (TXNIP). To investigate the activation of the inflammasome, we confirmed the mRNA and protein expression levels of the NLR family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and caspase-1 (CASP-1). Moreover, we confirmed that caspase mediates the mature form of interleukin-18, and the cleaved form of Gasdermin D (GSDMD) was increased. Based on these results, our study suggests that DON can induce damage through oxidative stress and pyroptosis in the epithelial cells of the porcine small intestine via NLRP3 inflammasome.
Keyphrases
- nlrp inflammasome
- oxidative stress
- induced apoptosis
- diabetic rats
- cell death
- cell cycle arrest
- endoplasmic reticulum stress
- dna damage
- weight loss
- ischemia reperfusion injury
- signaling pathway
- binding protein
- heavy metals
- bariatric surgery
- weight gain
- drinking water
- body mass index
- adipose tissue
- protein kinase
- irritable bowel syndrome
- high glucose
- replacement therapy
- combination therapy
- risk assessment
- clostridium difficile
- cell proliferation