| Cytokine modulation of Na(+)-dependent glutamine transport across the brush border membrane of monolayers of human intestinal Caco-2 cells. | |
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MedLine Citation:
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PMID: 1616390 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Previous studies have demonstrated that Na(+)-dependent brush border glutamine transport is diminished in septic patients. To examine the potential regulation of this decreased transport by endotoxin, cytokines, or glucocorticoids, the human intestinal Caco-2 cell line was studied in vitro. Na(+)-dependent glutamine transport across the apical brush border membrane was assayed in confluent monolayers of differentiated cells that were 10 days old. Uptake of 50 microM glutamine was determined after a 12-hour incubation with varying doses (10 to 1000 U/mL) of tumor necrosis factor-alpha, interleukin-1, interleukin-6, interferon-gamma, and various combinations of these cytokines. Studies were also done in cells incubated with E. coli endotoxin (1 micrograms/mL) or dexamethasone (1 and 10 microM). Endotoxin, tumor necrosis factor, interleukin-1, and interleukin-6 alone and in combination did not significantly reduce Na(+)-dependent glutamine transport across the brush border of Caco-2 cells. Dexamethasone decreased glutamine transport by 20%, but this decrease was not apparent for 48 hours. Interferon consistently decreased glutamine transport by 30%; this was due to a reduction in carrier maximal transport velocity (3427 +/- 783 pmol/mg protein/minute in controls versus 2279 +/- 411 in interferon, p less than 0.05) rather than a change in Km (276 +/- 29 microM in controls versus 333 +/- 74 in interferon, p = not interferon + dexamethasone + tumor necrosis factor + interleukin-1 resulted in a 38% decrease in transport activity. Cytokines and glucocorticoids may work independently and synergistically in regulating Na(+)-dependent brush border glutamine transport in human intestinal cells. Whether these signal molecules play a central role in the cause of the diminished brush border glutamine transport that occurs in septic patients requires further study. |
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Authors:
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W W Souba; E M Copeland |
Publication Detail:
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Type: In Vitro; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Annals of surgery Volume: 215 ISSN: 0003-4932 ISO Abbreviation: Ann. Surg. Publication Date: 1992 May |
Date Detail:
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Created Date: 1992-07-30 Completed Date: 1992-07-30 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 0372354 Medline TA: Ann Surg Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 536-44; discussion 544-5 Citation Subset: AIM; IM |
Affiliation:
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Department of Surgery, University of Florida College of Medicine, Gainesville. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenocarcinoma
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pathology Biological Transport, Active / physiology Colonic Neoplasms / pathology Cytokines / physiology* Dexamethasone / pharmacology Endotoxins / pharmacology Glutamine / metabolism* Humans Microvilli / metabolism Sodium / metabolism* Tumor Cells, Cultured / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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CA-45237/CA/NCI NIH HHS; HL-44986/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Endotoxins; 50-02-2/Dexamethasone; 56-85-9/Glutamine; 7440-23-5/Sodium |
| Comments/Corrections | |
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