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Article: Modulation of mucin mRNA (MUC5AC and MUC5B) expression and protein production and secretion in Caco-2/HT29-MTX co-cultures following exposure to individual and combined Fusarium mycotoxins.

TitleModulation of mucin mRNA (MUC5AC and MUC5B) expression and protein production and secretion in Caco-2/HT29-MTX co-cultures following exposure to individual and combined Fusarium mycotoxins.
Authors
KeywordsDeoxynivalenol
Fumonisin B1
Intestinal epithelia
Mucins
Nivalenol
Zearalenone
Issue Date2014
PublisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/
Citation
Toxicol Science, 2014, v. 139 n. 1, p. 83-98 How to Cite?
AbstractIntestinal epithelial cells (IECs) are a critical component of the innate local immune response. In order to reduce the risk of pathogen infection or xenobiotic intoxication, different host defense mechanisms have been evolved. Evidence has shown that upon ingestion of food or feed contaminated with toxins (e.g., mycotoxins), IECs respond by regulating mucin secretions, which act as a physical barrier inhibiting bacterial attachment and subsequent infection-related processes. However, the effect of Fusarium mycotoxins on mucin production remains unclear. Consequently, the aim of this study was to evaluate individual and interactive effects of four common Fusarium mycotoxins, deoxynivalenol, nivalenol, zearalenone, and fumonisins B1 on mRNA expression and secretion of mucins, MUC5AC, and MUC5B, as well as total mucin-like glycoprotein secretion, using Caco-2 (absorptive-type) and HT29-MTX (secretive-type) cells and their co-cultures (initial seeding ratios Caco-2/HT29-MTX: 90/10 and 70/30). Our results showed that individual and mixtures of mycotoxins significantly modulated MUC5AC and MUC5B mRNA and protein, and total mucin-like glycoprotein secretion as measured by quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, and enzyme-linked lectin assay, respectively. Additive effects were not always observed for mixtures. Also, the present study showed that in co-cultures, lower MUC5AC and MUC5B mRNA, protein and total mucin production occurred following exposure, which might suggest higher intestinal permeability and susceptibility to toxin exposure. This study demonstrates the importance of selecting an appropriate cell model for the in vitro investigation of Fusarium mycotoxin effects either alone or in combinations on the immunological defense mechanisms of IECs, and will contribute to improved toxin risk assessments.
Persistent Identifierhttp://hdl.handle.net/10722/201546
ISSN
2023 Impact Factor: 3.4
2023 SCImago Journal Rankings: 0.911
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWan, MLYen_US
dc.contributor.authorAllen, KJen_US
dc.contributor.authorTurner, PCen_US
dc.contributor.authorEl-Nezamy, Hen_US
dc.date.accessioned2014-08-21T07:30:24Z-
dc.date.available2014-08-21T07:30:24Z-
dc.date.issued2014en_US
dc.identifier.citationToxicol Science, 2014, v. 139 n. 1, p. 83-98en_US
dc.identifier.issn1096-6080-
dc.identifier.urihttp://hdl.handle.net/10722/201546-
dc.description.abstractIntestinal epithelial cells (IECs) are a critical component of the innate local immune response. In order to reduce the risk of pathogen infection or xenobiotic intoxication, different host defense mechanisms have been evolved. Evidence has shown that upon ingestion of food or feed contaminated with toxins (e.g., mycotoxins), IECs respond by regulating mucin secretions, which act as a physical barrier inhibiting bacterial attachment and subsequent infection-related processes. However, the effect of Fusarium mycotoxins on mucin production remains unclear. Consequently, the aim of this study was to evaluate individual and interactive effects of four common Fusarium mycotoxins, deoxynivalenol, nivalenol, zearalenone, and fumonisins B1 on mRNA expression and secretion of mucins, MUC5AC, and MUC5B, as well as total mucin-like glycoprotein secretion, using Caco-2 (absorptive-type) and HT29-MTX (secretive-type) cells and their co-cultures (initial seeding ratios Caco-2/HT29-MTX: 90/10 and 70/30). Our results showed that individual and mixtures of mycotoxins significantly modulated MUC5AC and MUC5B mRNA and protein, and total mucin-like glycoprotein secretion as measured by quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, and enzyme-linked lectin assay, respectively. Additive effects were not always observed for mixtures. Also, the present study showed that in co-cultures, lower MUC5AC and MUC5B mRNA, protein and total mucin production occurred following exposure, which might suggest higher intestinal permeability and susceptibility to toxin exposure. This study demonstrates the importance of selecting an appropriate cell model for the in vitro investigation of Fusarium mycotoxin effects either alone or in combinations on the immunological defense mechanisms of IECs, and will contribute to improved toxin risk assessments.-
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/en_US
dc.relation.ispartofToxicol Scienceen_US
dc.rightsToxicol Science. Copyright © Oxford University Press.-
dc.rightsAuthor holds the copyright-
dc.subjectDeoxynivalenol-
dc.subjectFumonisin B1-
dc.subjectIntestinal epithelia-
dc.subjectMucins-
dc.subjectNivalenol-
dc.subjectZearalenone-
dc.subject.meshFusarium - chemistry-
dc.subject.meshMucin 5AC - genetics-
dc.subject.meshMucin-5B - genetics-
dc.subject.meshMycotoxins - toxicity-
dc.subject.meshRNA, Messenger - genetics-
dc.titleModulation of mucin mRNA (MUC5AC and MUC5B) expression and protein production and secretion in Caco-2/HT29-MTX co-cultures following exposure to individual and combined Fusarium mycotoxins.en_US
dc.typeArticleen_US
dc.identifier.emailWan, LY: murphyly@hku.hken_US
dc.identifier.emailEl-Nezamy, H: elnezami@hkucc.hku.hken_US
dc.identifier.authorityEl-Nezamy, H=rp00694en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/toxsci/kfu019en_US
dc.identifier.pmid24496642-
dc.identifier.scopuseid_2-s2.0-84896703971-
dc.identifier.hkuros232332en_US
dc.identifier.volume139en_US
dc.identifier.issue1-
dc.identifier.spage83en_US
dc.identifier.epage98en_US
dc.identifier.isiWOS:000335144600008-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl1096-0929-

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