Ozkan A N, Hoyt D B, Ninnemann J L, Mitchell M D
Department of Reproductive Medicine, University of California Medical Center, San Diego 92103.
Immunol Lett. 1988 Jan;17(1):79-83. doi: 10.1016/0165-2478(88)90105-8.
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.
将外周血黏附单核细胞或羊膜细胞在体外暴露于纳摩尔量的创伤相关免疫抑制肽，会导致前列腺素E2（PGE2）的生物合成增加。与缓冲液对照相比，创伤肽使前列腺素E2的生物合成增加了多达425%。将创伤肽添加到混合淋巴细胞培养物中，可显著抑制人外周血淋巴细胞对[3H]胸苷的掺入。向混合淋巴细胞培养物中添加吲哚美辛（一种前列腺素生物合成抑制剂）并不能显著消除该肽的免疫抑制活性。这些结果表明，创伤肽对T淋巴细胞母细胞生成的抑制可能至少由两种机制介导：（1）通过创伤肽诱导的PGE2生物合成增加，以及（2）通过非环氧化酶介导的途径。
