Abstract |
In vitro exposure of peripheral-blood-adherent mononuclear cells or amnion cells to nanomolar quantities of a trauma-associated immunosuppressive peptide resulted in an increased biosynthesis of prostaglandin E2 ( PGE2). Trauma peptide enhanced prostaglandin E2 biosynthesis by as much as 425% compared to buffer controls. The addition of trauma peptide to mixed lymphocyte cultures significantly inhibited [3H] thymidine incorporation by human peripheral blood lymphocytes. Addition of indomethacin (an inhibitor of prostaglandin biosynthesis) to mixed lymphocyte cultures did not significantly abrogate the immunosuppressive activity of the peptide. These results indicate that suppression of T lymphocyte blastogenesis by trauma peptide is probably mediated by at least two mechanisms: (1) by increased PGE2 biosynthesis, induced by trauma peptide, and (2) through a non- cyclooxygenase-mediated pathway.
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Authors | A N Ozkan, D B Hoyt, J L Ninnemann, M D Mitchell |
Journal | Immunology letters
(Immunol Lett)
Vol. 17
Issue 1
Pg. 79-83
(Jan 1988)
ISSN: 0165-2478 [Print] Netherlands |
PMID | 2965105
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Glycopeptides
- Prostaglandins E
- suppressor active peptide (thermal injury)
- Polymyxin B
- Dinoprostone
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Topics |
- Dinoprostone
- Glycopeptides
(immunology, pharmacology)
- Humans
- Immunosuppression Therapy
- In Vitro Techniques
- Leukocytes, Mononuclear
(drug effects, metabolism)
- Lymphocyte Culture Test, Mixed
- Polymyxin B
(pharmacology)
- Prostaglandins E
(biosynthesis, immunology, pharmacology)
- Wounds and Injuries
(immunology)
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