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- W2057194771 abstract "Certain arachidonic acid metabolites, including prostaglandins (PGs) E1 and E2, have been shown to exert marked immunosuppressive effects on T-cell and macrophage functions. Cyclooxygenase blockade with indomethacin or ibuprofen may ameloriate these effects. In the current study we measured lymphocyte proliferation by thymidine incorporation, the presence of T-cell activation antigens with monoclonal antibodies and two-color flow cytometry, and neutrophil (PMN) oxidative burst using a fluorescent marker, in control mice and in burned mice treated with indomethacin for 10 days after injury. One-half of the cell cultures were treated with indomethacin in vitro to ensure its continued presence during stimulation. Separate groups of mice were fed a fish oil-based diet which leads to the production of PGE3 rather than PGE2, versus standard mouse chow, a soy-bean oil-based diet which leads to PGE2 production. Lymphocyte proliferation, expression of T-cell activation antigens, and PMN oxidative burst remained depressed in burned mice treated with indomethacin in vivo (plus in vitro) and in those which received the fish oil-based diet, compared to control. Blockade of PG synthesis after murine burn injury by cyclooxygenase inhibition or alterations in the diet failed to restore T-lymphocyte activation or proliferation or to improve PMN oxidative burst. These data suggest that PGE2 alone does not explain the immunosuppression noted after burn injury." @default.
- W2057194771 created "2016-06-24" @default.
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- W2057194771 date "1990-01-01" @default.
- W2057194771 modified "2023-10-08" @default.
- W2057194771 title "Postburn suppression of murine lymphocyte and neutrophil functions is not reversed by prostaglandin blockade" @default.
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- W2057194771 doi "https://doi.org/10.1016/0022-4804(90)90151-q" @default.
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