About: Nontoxic-dose deoxynivalenol aggravates lipopolysaccharides-induced inflammation and tight junction disorder in IPEC-J2 cells through activation of NF-κB and LC3B

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About: Nontoxic-dose deoxynivalenol aggravates lipopolysaccharides-induced inflammation and tight junction disorder in IPEC-J2 cells through activation of NF-κB and LC3B Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Nontoxic-dose deoxynivalenol aggravates lipopolysaccharides-induced inflammation and tight junction disorder in IPEC-J2 cells through activation of NF-κB and LC3B
Creator	Huang, Kehe Liu, Shuiping Gan, Fang Hou, Lili Liu, Dandan Ge, Lei Le, Guannan Lin, Ziman Mao, Xinru
source	PMC
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.
has issue date	2020-08-30(xsd:dateTime)
bibo:doi	10.1016/j.fct.2020.111712
has license	no-cc
schema:url	https://doi.org/10.1016/j.fct.2020.111712
resource representing a document's title	Nontoxic-dose deoxynivalenol aggravates lipopolysaccharides-induced inflammation and tight junction disorder in IPEC-J2 cells through activation of NF-κB and LC3B
has PubMed Central identifier	PMC7456579
schema:publication	Food Chem Toxicol
resource representing a document's body	covid:PMC7456579#body_text
is schema:about of	named entity 'lipopolysaccharides' named entity 'tight junction' named entity 'inflammasome' named entity 'paraformaldehyde' named entity 'mycotoxins' named entity 'Pierron' named entity 'NF-κB' named entity 'SPSS' named entity 'CO2' named entity 'plasmid' named entity 'protein' named entity 'signaling pathway' named entity 'LC3B' named entity 'cytokines' named entity 'IL-6' named entity 'ZO-1' named entity 'protein' named entity 'western blotting' named entity 'inflammation' named entity 'inflammatory response' named entity 'LC3B' named entity 'IκB' named entity 'LC3B' named entity 'tight junction' named entity 'LPS' named entity 'significantly increased' named entity 'China' named entity 'LPS' named entity 'LPS' named entity 'epithelial cells' named entity 'tight junction' named entity 'cell incubator' named entity 'mRNA' named entity 'DMSO' named entity 'gut microbiota' named entity 'formazan' named entity 'Abcam' named entity 'NF-κB' named entity 'mycotoxin' named entity '0.01' named entity 'NLRP3' named entity 'ultrasonic' named entity 'fetal bovine serum' named entity 'LPS' named entity 'inflammation' named entity 'E. coli' named entity 'protein' named entity 'microbiota' named entity 'receptor' named entity 'intestinal disease' named entity 'secondary metabolites' named entity 'C57BL/6J' named entity 'cell wall' named entity 'Data curation' named entity 'p65' named entity 'Aflatoxin' named entity 'epithelial' named entity 'pro-inflammatory cytokines' named entity 'LPS' named entity 'PBS' named entity 'clones' named entity 'expression levels' named entity 'tight junction' named entity 'inflammation' named entity 'connection form' named entity 'NLRP3' named entity 'inflammasome' named entity 'protein expression' named entity 'IBS' named entity 'LC3B' named entity 'inflammatory markers' named entity 'phosphorylation' named entity 'TNF-α' named entity 'NLRP3' named entity 'basic treatment' named entity 'inflammatory cytokines'

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