| pubmed-article:8450217 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C0221908 | lld:lifeskim |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C0040223 | lld:lifeskim |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C1149169 | lld:lifeskim |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C0750729 | lld:lifeskim |
| pubmed-article:8450217 | lifeskim:mentions | umls-concept:C0173022 | lld:lifeskim |
| pubmed-article:8450217 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:8450217 | pubmed:dateCreated | 1993-4-13 | lld:pubmed |
| pubmed-article:8450217 | pubmed:abstractText | The single cell-thick intestinal epithelium forms a crucial barrier between the host and environment, and is modeled in vitro by a monolayer of polarized, highly differentiated T84 epithelial cells impermeable to most macromolecules because of functional intercellular tight junctions. Absence of a permeability defect across the monolayer, either transcellular or paracellular, is indicated by development of a transepithelial electrical resistance of > or = 1000 ohm-cm2, reported to be markedly diminished by exposure to a T lymphocyte cytokine, IFN-gamma. We sought to define this phenomenon in four ways by determining its duration and reversibility; the uniqueness of type II (gamma) IFN as opposed to type I (alpha) IFN; the surface of the polarized columnar epithelium likely involved in responding to IFN-gamma; and whether a specific surface membrane receptor on the epithelial cell participates in the response. Using a special apparatus that allows differential cytokine exposure of monolayer surfaces, our data demonstrate 1) only the monolayer's basolateral surface is IFN-gamma responsive, whereas the apical (microvillous) surface is no; 2) the alteration in electrical resistance of epithelium is prolonged (5 days), even after a single (24 h) exposure to IFN-gamma, but nevertheless is reversible; 3) the effect is likely receptor-ligand mediated, because it can be partially blocked by IFN-gamma receptor-specific monoclonal Ig; 4) an alteration in tight junction function (a paracellular pathway) rather than cell necrosis or a transcellular pathway is responsible for IFN-gamma-induced monolayer dysfunction because permeability to a 44,000-Da macromolecule (horseradish peroxidase) did not increase, and intracytoplasmic T84 cell enzymes were not released into the media; and 5) the biologic phenomenon could not be induced by a species (alpha) of class I IFN, making IFN-gamma reasonably unique in this regard. Given the proximity; activation status, and capacity of T lymphocytes for cytokine production in mucosa, we suggest that IFN-gamma-induced changes in epithelial permeability may be a major cause of altered intestinal barrier function in vivo. | lld:pubmed |
| pubmed-article:8450217 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8450217 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8450217 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8450217 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:8450217 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8450217 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8450217 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:8450217 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:8450217 | pubmed:author | pubmed-author:AdamsR BRB | lld:pubmed |
| pubmed-article:8450217 | pubmed:author | pubmed-author:RocheJ KJK | lld:pubmed |
| pubmed-article:8450217 | pubmed:author | pubmed-author:PlanchonS MSM | lld:pubmed |
| pubmed-article:8450217 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8450217 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:8450217 | pubmed:volume | 150 | lld:pubmed |
| pubmed-article:8450217 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8450217 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8450217 | pubmed:pagination | 2356-63 | lld:pubmed |
| pubmed-article:8450217 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:8450217 | pubmed:meshHeading | pubmed-meshheading:8450217-... | lld:pubmed |
| pubmed-article:8450217 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8450217 | pubmed:articleTitle | IFN-gamma modulation of epithelial barrier function. Time course, reversibility, and site of cytokine binding. | lld:pubmed |
| pubmed-article:8450217 | pubmed:affiliation | Department of Surgery, University of Virginia Health Sciences Center, Charlottesville 22908. | lld:pubmed |
| pubmed-article:8450217 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8450217 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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