Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-12
pubmed:abstractText
The effects of physiologically relevant increase in temperature (37-41 degrees C) on intestinal epithelial tight junction (TJ) barrier have not been previously studied. Additionally, the role of heat-shock proteins (HSPs) in the regulation of intestinal TJ barrier during heat stress remains unknown. Because heat-induced disturbance of intestinal TJ barrier could lead to endotoxemia and bacterial translocation during physiological thermal stress, the purpose of this study was to investigate the effects of modest, physiologically relevant increases in temperature (37-41 degrees C) on intestinal epithelial TJ barrier and to examine the protective role of HSPs on intestinal TJ barrier. Filter-grown Caco-2 intestinal epithelial cells were used as an in vitro intestinal epithelial model system to assess the effects of heat exposure on intestinal TJ barrier. Exposure of filter-grown Caco-2 monolayers to modest increases in temperatures (37-41 degrees C) resulted in a significant time- and temperature-dependent increases in Caco-2 TJ permeability. Exposure to modest heat (39 or 41 degrees C) resulted in rapid and sustained increases in HSP expression; and inhibition of HSP expression produced a marked increase in heat-induced increase in Caco-2 TJ permeability (P < 0.001). Heat exposure (41 degrees C) resulted in a compensatory increase in Caco-2 occludin protein expression and an increase in junctional localization. Inhibition of HSP expression prevented the compensatory upregulation of occludin protein expression and produced a marked disruption in junctional localization of occludin protein during heat stress. In conclusion, our findings demonstrate for the first time that a modest, physiologically relevant increase in temperature causes an increase in intestinal epithelial TJ permeability. Our data also show that HSPs play an important protective role in preventing the heat-induced disruption of intestinal TJ barrier and suggest that HSP mediated upregulation of occludin expression may be an important mechanism involved in the maintenance of intestinal epithelial TJ barrier function during heat stress.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0193-1857
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G204-12
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16407590-Actins, pubmed-meshheading:16407590-Apoptosis, pubmed-meshheading:16407590-Blotting, Western, pubmed-meshheading:16407590-Caco-2 Cells, pubmed-meshheading:16407590-Cell Death, pubmed-meshheading:16407590-Cycloheximide, pubmed-meshheading:16407590-HSP70 Heat-Shock Proteins, pubmed-meshheading:16407590-Heat-Shock Proteins, pubmed-meshheading:16407590-Hot Temperature, pubmed-meshheading:16407590-Humans, pubmed-meshheading:16407590-Immunohistochemistry, pubmed-meshheading:16407590-Intestinal Absorption, pubmed-meshheading:16407590-Intestinal Mucosa, pubmed-meshheading:16407590-Membrane Proteins, pubmed-meshheading:16407590-Permeability, pubmed-meshheading:16407590-Protein Synthesis Inhibitors, pubmed-meshheading:16407590-Temperature, pubmed-meshheading:16407590-Tight Junctions
pubmed:year
2006
pubmed:articleTitle
Physiologically relevant increase in temperature causes an increase in intestinal epithelial tight junction permeability.
pubmed:affiliation
Internal Medicine-Gastroenterology and Hepatology, University of New Mexico, Albuquerque, New Mexico 87131-0001, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural