| Mechanism of intestinal-derived fungal sepsis by gliotoxin, a fungal metabolite. | |
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MedLine Citation:
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PMID: 12778404 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND/PURPOSE: Gut barrier dysfunction resulting from fungal overgrowth may be caused by the interaction of gliotoxin (GT), a fungal metabolite, with enterocytes. The goal of this study was to determine the mechanisms by which gliotoxin (GT), a fungal metabolite, causes enterocyte apoptosis. METHODS: The authors measured enterocyte apoptosis, caspase-3 activity, pro-caspase-3, and poly (ADP-ribose) polymerase (PARP) cleavage in GT-exposed IEC-6 cells, a rat intestinal cell line. RESULTS: GT induced apoptosis in IEC-6 cells. The pan-caspase inhibitor ZVAD suppressed this GT-mediated apoptosis. GT induced a 15-fold increase in caspase-3 activity over media control. The authors detected PARP cleavage by after GT exposure. DTT pretreatment decreased apoptosis compared with GT alone. CONCLUSIONS: This study supports the concept that fungal overgrowth may lead to gut barrier dysfunction by the local release of gliotoxin and the induction enterocyte apoptosis. |
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Authors:
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Jeffrey S Upperman; Douglas A Potoka; Xiao-Ru Zhang; Katerina Wong; Ruben Zamora; Henri R Ford |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of pediatric surgery Volume: 38 ISSN: 1531-5037 ISO Abbreviation: J. Pediatr. Surg. Publication Date: 2003 Jun |
Date Detail:
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Created Date: 2003-06-02 Completed Date: 2003-10-03 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0052631 Medline TA: J Pediatr Surg Country: United States |
Other Details:
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Languages: eng Pagination: 966-70 Citation Subset: IM |
Affiliation:
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Department of Surgery, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology Candidiasis / microbiology, pathology Cell Line Dose-Response Relationship, Drug Gliotoxin / antagonists & inhibitors, blood, metabolism*, toxicity* Intestinal Diseases / microbiology*, pathology Rats Sepsis / microbiology*, pathology Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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1K08 GM00696 01/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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67-99-2/Gliotoxin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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