pubmed-article:1893631 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1893631 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:1893631 | lifeskim:mentions | umls-concept:C0227354 | lld:lifeskim |
pubmed-article:1893631 | lifeskim:mentions | umls-concept:C0596873 | lld:lifeskim |
pubmed-article:1893631 | lifeskim:mentions | umls-concept:C0053398 | lld:lifeskim |
pubmed-article:1893631 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:1893631 | pubmed:dateCreated | 1991-10-24 | lld:pubmed |
pubmed-article:1893631 | pubmed:abstractText | BCM is a milk-derived peptide with opiate-like properties which is absorbed through the gastrointestinal mucosa. It has been shown to affect gastrointestinal motility, absorption and secretion. Recently, modulation of the immune system by BCM was also reported. In this study we investigated the in vitro effect of BCM on the human mucosal immune response as represented by lamina propria lymphocyte (LPL) proliferation. Results show that BCM significantly inhibited concanavalin A (ConA) stimulated LPL DNA synthesis. BCM also inhibited ornithine decarboxylase activity (ODC) in ConA-stimulated LPL. Although BCM also inhibited 12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulated LPL DNA synthesis, the degree of inhibition was much lower than in ConA-stimulated LPL. The anti-proliferative effect of BCM was reversed by the opiate receptor antagonist, neloxone. Our results suggest that BCM may affect the human mucosal immune system, possibly via the opiate receptor. | lld:pubmed |
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pubmed-article:1893631 | pubmed:language | eng | lld:pubmed |
pubmed-article:1893631 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1893631 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1893631 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1893631 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1893631 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1893631 | pubmed:month | Sep | lld:pubmed |
pubmed-article:1893631 | pubmed:issn | 0009-9104 | lld:pubmed |
pubmed-article:1893631 | pubmed:author | pubmed-author:LukG DGD | lld:pubmed |
pubmed-article:1893631 | pubmed:author | pubmed-author:ElitsurYY | lld:pubmed |
pubmed-article:1893631 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1893631 | pubmed:volume | 85 | lld:pubmed |
pubmed-article:1893631 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1893631 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1893631 | pubmed:pagination | 493-7 | lld:pubmed |
pubmed-article:1893631 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:1893631 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1893631 | pubmed:articleTitle | Beta-casomorphin (BCM) and human colonic lamina propria lymphocyte proliferation. | lld:pubmed |
pubmed-article:1893631 | pubmed:affiliation | Department of Pediatrics, Wayne State University, Detroit, MI. | lld:pubmed |
pubmed-article:1893631 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1893631 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1893631 | lld:pubmed |