Linked Life Data

20956974

Source:http://linkedlifedata.com/resource/pubmed/id/20956974

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-2-1
pubmed:abstractText
Yersinia enterocolitica is a common cause of acute gastroenteritis. This study aimed to clarify the mechanisms leading to barrier dysfunction and diarrhea. Exposure of human colonic HT-29/B6 cells to Y. enterocolitica resulted in a decrease in transepithelial resistance from 404±23 to 163±21 ? cm² (P<0.001) in parallel with an increase in mannitol (182?Da) and fluorescein (332?Da) permeability, whereas short circuit current did not change. This effect was time dependent, required the presence of living bacteria, could not be triggered by bacterial supernatants and was not due to Yersinia outer proteins. Concomitantly, Y. enterocolitica induced necrosis as indicated by an increase in lactate dehydrogenase-release, whereas epithelial apoptosis was not upregulated. Local changes in conductivity were detected by conductance scanning, indicating 'leaky regions' within the epithelium that were visualized by biotinylation and confocal microscopy. In these regions, claudin-3 and -4 and, especially claudin-8, were redistributed off the tight junction (TJ) into the cytoplasm. In addition, the expression of claudin-2, -3, -8, -10 and ZO-1 was diminished as quantified by immunoblotting. Moreover, we found claudin-8 to be regulated by the c-Jun N-terminal kinase, the inhibition of which attenuated the Y. enterocolitica-induced decrease in transepithelial resistance and restored claudin-8 protein level. In conclusion, barrier dysfunction in Y. enterocolitica infection is due to circumscribed epithelial TJ protein changes and necrotic cell loss, as a consequence of which leak flux diarrhea and antigen-uptake provoking extraintestinal arthritis may be triggered.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1530-0307
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
310-24
pubmed:meshHeading
pubmed-meshheading:20956974-Calcium, pubmed-meshheading:20956974-Cell Line, pubmed-meshheading:20956974-Claudins, pubmed-meshheading:20956974-Colon, pubmed-meshheading:20956974-Diarrhea, pubmed-meshheading:20956974-Dielectric Spectroscopy, pubmed-meshheading:20956974-Electric Impedance, pubmed-meshheading:20956974-Epithelium, pubmed-meshheading:20956974-Fluorescein, pubmed-meshheading:20956974-Humans, pubmed-meshheading:20956974-Immunoblotting, pubmed-meshheading:20956974-In Situ Nick-End Labeling, pubmed-meshheading:20956974-L-Lactate Dehydrogenase, pubmed-meshheading:20956974-Mannitol, pubmed-meshheading:20956974-Microscopy, Electron, pubmed-meshheading:20956974-Necrosis, pubmed-meshheading:20956974-Permeability, pubmed-meshheading:20956974-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20956974-Tight Junctions, pubmed-meshheading:20956974-Yersinia enterocolitica
pubmed:year
2011
pubmed:articleTitle
Yersinia enterocolitica induces epithelial barrier dysfunction through regional tight junction changes in colonic HT-29/B6 cell monolayers.
pubmed:affiliation
Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité Campus Benjamin Franklin, Berlin, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't