ArticleFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association2020
Nontoxic-dose deoxynivalenol aggravates lipopolysaccharides-induced inflammation and tight junction disorder in IPEC-J2 cells through activation of NF-κB and LC3B.
Article in Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Deoxynivalenol-induced cellular signal transduction: research progress on toxicological effects, molecular mechanisms, and biological intervention strategies.Molecular biology reports · 2026Review
- Glutamine alleviates feed restriction-induced barrier function injury in yak rumen epithelium.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Bacillus velezensis mitigates deoxynivalenol-induced intestinal inflammation and liver injury via modulating the gut microbiota.NPJ science of food · 2026Article
- Lycopene Protects Deoxynivalenol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation by Targeting the ERK Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- The Novel Role of the NLRP3 Inflammasome in Mycotoxin-Induced Toxicological Mechanisms.Veterinary sciences · 2024Review
- Article
- Constitutively active microglial populations limit anorexia induced by the food contaminant deoxynivalenol.Journal of neuroinflammation · 2022Article
- Zearalenone Promotes LPS-Induced Oxidative Stress, Endoplasmic Reticulum Stress, and Accelerates Bovine Mammary Epithelial Cell Apoptosis.International journal of molecular sciences · 2022Article
- Phenethyl isothiocyanate as an anti-nutritional factor attenuates deoxynivalenol-induced IPEC-J2 cell injury through inhibiting ROS-mediated autophagy.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2022Article
- Article
- Secondary Dysfunction of the Intestinal Barrier in the Pathogenesis of Complications of Acute Poisoning.Journal of evolutionary biochemistry and physiology · 2022Article
- Melatonin Ameliorates LPS-Induced Testicular Nitro-oxidative Stress (iNOS/TNFα) and Inflammation (NF-kB/COX-2) via Modulation of SIRT-1.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Ochratoxin A induces nephrotoxicity in vitro and in vivo via pyroptosis.Archives of toxicology · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS) is the key factor in various intestinal inflammation which could disrupt the epithelial barrier function. Deoxynivalenol (DON), a well-known mycotoxin, can induce intestinal injury. However, the combined enterotoxicity of LPS and DON has rarely been studied. In this study, IPEC-J2 cell monolayers were exposed to LPS and nontoxic-dose DON for 12 and 24 h to investigate the effects of DON on LPS-induced inflammatory response and tight junction variation, and specific inhibitor and CRISPR-Cas9 were used to explore the underlying mechanisms. Our results showed that nontoxic-dose DON aggravated LPS-induced cellular inflammatory response, reflecting on more significant changes of inflammatory cytokines mRNA expression, higher protein expression of NOD-like receptor protein 3 (NLRP3) and procaspase-1. Moreover, nontoxic-dose DON aggravated LPS-induced mRNA and protein expression decreased, and distribution confused of tight junction proteins. We found that DON further enhanced LPS-induced phosphorylation and nucleus translocation of p65, and expression of LC3B-Ⅱ. NF-κB inhibitor and CRISPR-Cas9-mediated knockout of LC3B attenuated the effects of combination which indicated nontoxic-dose DON aggravated LPS-induced intestinal inflammation and tight junction disorder through activating NF-κB signaling pathway and autophagy-related protein LC3B. It further warns that ingesting low doses of mycotoxins may exacerbate the effects of intestinal pathogens on the body.
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