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BibTeX
LPS Induces Hyper‐Permeability of Intestinal Epithelial Cells
Journal of cellular physiology, 2017-02, Vol.232 (2), p.381-390
Bein, Amir
Zilbershtein, Alexander
Golosovsky, Michael
Davidov, Dan
Schwartz, Betty
2017
Details
Autor(en) / Beteiligte
Bein, Amir
Zilbershtein, Alexander
Golosovsky, Michael
Davidov, Dan
Schwartz, Betty
Titel
LPS Induces Hyper‐Permeability of Intestinal Epithelial Cells
Ist Teil von
Journal of cellular physiology, 2017-02, Vol.232 (2), p.381-390
Ort / Verlag
United States: Wiley Subscription Services, Inc
Erscheinungsjahr
2017
Link zum Volltext
Quelle
Wiley Online Library
Beschreibungen/Notizen
Necrotizing Enterocolitis (NEC) is a severe inflammatory disorder leading to high morbidity and mortality rates. A growing body of evidence demonstrate the key role of the Toll like receptor 4 (TLR4) in NEC. This membranal receptor recognizes lipopolysaccharides (LPS) from the bacterial wall and triggers an inflammatory response. The aim of the present study was to elucidate the effect of LPS on paracellular permeability known to be severely affected in NEC. IEC‐18 cells were treated with LPS and the effects on morphology, paracellular permeability and their associated gene and protein expressions were measured. Our results show that LPS down regulated the expression of occludin and ZO‐1 mRNAs while up regulating Cdkn1a. In addition LPS caused a significant increase in paracellular permeability and epithelial barrier damage. Finally ZO‐1 protein was found to be spatially disarrayed in the intercellular junctions in response to LPS. We conclude that LPS adversely affected the functionality of the intestinal epithelial barrier suggesting a new mechanism by which bacterial infection may contribute to the development of NEC. J. Cell. Physiol. 232: 381–390, 2017. © 2016 Wiley Periodicals, Inc. This study explores the effect of LPS on paracellular permeability known to be severely affected in NEC. We show that LPS adversely affected the functionality of the intestinal epithelial barrier and in particular led to spatial disarrangement of ZO‐1 protein.
Sprache
Englisch
Identifikatoren
ISSN: 0021-9541
eISSN: 1097-4652
DOI: 10.1002/jcp.25435
Titel-ID: cdi_proquest_miscellaneous_1826682794
Format
–
Schlagworte
Cell Line
,
Cell Membrane Permeability - drug effects
,
Epithelial Cells - cytology
,
Epithelial Cells - drug effects
,
Epithelial Cells - ultrastructure
,
Gene Expression Regulation - drug effects
,
Humans
,
Intestines - cytology
,
Lipopolysaccharides - pharmacology
,
NF-kappa B - metabolism
,
Signal Transduction - drug effects
,
Surface Plasmon Resonance
,
Tight Junctions - drug effects
,
Tight Junctions - metabolism
,
Tight Junctions - ultrastructure
,
Toll-Like Receptor 4 - metabolism
,
Zonula Occludens-1 Protein - metabolism
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