2. Academic Validation
  3. Fumonisin B1 induced intestinal epithelial barrier damage through endoplasmic reticulum stress triggered by the ceramide synthase 2 depletion

Fumonisin B1 induced intestinal epithelial barrier damage through endoplasmic reticulum stress triggered by the ceramide synthase 2 depletion

  • Food Chem Toxicol. 2022 Aug;166:113263. doi: 10.1016/j.fct.2022.113263.
Mengcong Li 1,  Shuhui Liu 1,  Lei Tan 2,  Yan Luo 2,  Zhangshan Gao 1,  Jiwen Liu 1,  Yuting Wu 1,  Wentao Fan 1,  Sarah DeSaeger 3,  Suquan Song 4
Affiliations

Affiliations

  • 1 MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
  • 2 Administration for Market Regulation of Guangdong Province Key Laboratory of Supervision for Edible Agricultural Products, Shenzhen Centre of Inspection and Testing for Agricultural Products, Shenzhen, 518000, China.
  • 3 Centre of Excellence in Mycotoxicology and Public Health, Department of Bioanalysis, Faculty of Pharmaceutical Sciences, Ghent University, Ottergemsesteenweg 460, B-9000, Ghent, Belgium.
  • 4 MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China. Electronic address: suquan.song@njau.edu.cn.
PMID: 35777715 DOI: 10.1016/j.fct.2022.113263
Abstract

Fumonisin B1 (FB1) contamination in feed is of great concern nowadays. The intestine would be the first line when FB1-contaminated food or feed was ingested. However, the intestinal toxicity and mechanism of FB1 have rarely been studied. In this study, we found that FB1 inhibited cell viability, and promoted the severe release of Lactate Dehydrogenase. Meantime, FB1 destroyed the intestinal physical barrier by reducing the expressions of tight junctions. And FB1 induced excessive production of cytokines like tumor necrosis factor-α, resulting in damage to the intestinal immunological barrier. Furthermore, we observed that FB1 preferentially inhibited the expressions of ceramide synthase 2 (CerS2) and upregulated the expression of endoplasmic reticulum (ER) stress markers. The siRNA-mediated knockdown of CerS2 and CerS2 overexpression proved that CerS2 depletion induced by FB1 triggered ER stress, which then destructed the intestinal barrier. FB1-induced intestinal impairment could be restored by CerS2 over-expression or 4-Phenylbutyric acid (ER stress inhibitor). Overall, our findings demonstrated intestinal toxicity and potential mechanism of FB1, and the intestinal impairment risk posed by FB1 must be taken seriously.

Keywords

Ceramide synthase; ER stress; Fumonisin B(1); Intestinal barrier.

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