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Ertel, W.* ; Faist, E.H.K.J.* ; Nestle, C.* ; Hueltner, L. ; Storck, M.* ; Schildberg -, F.W.*

Kinetics of interleukin-2 and interleukin-6 synthesis following major mechanical trauma.

J. Surg. Res. 48, 622-628 (1990)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Although it is known that mitogen-induced lymphocyte proliferation and interleukin-2 (IL-2) synthesis are depressed following mechanical trauma, it is not known whether these defects are due to high levels of circulating prostaglandin E2 released by macrophages, suppressor T-lymphocytes, and serum suppressive factors or due to intracellular defects in T-lymphocytes. Moreover, the kinetic of interleukin-6 (IL-6), a new multifunctional cytokine, following trauma is not known. To study this, highly purified T-cell cultures were prepared from 21 patients with major mechanical trauma on Days 3, 7, 10, 14, and 21 post-trauma and assayed for proliferative response to phytohemagglutinin, IL-2, and IL-6 synthesis. T-lymphocyte proliferation of patients was unaltered on all days post-trauma compared to that of healthy controls. Interleukin-2 synthesis of patients showed a significant (P < 0.01) reduction ranging from 23% of control values on Day 3 to 40% on Day 21. Interleukin-6 synthesis in contrast was markedly increased (P < 0.05) in the patient group on all days up to sixfold (Day 3) with a tendency toward normalization on Day 21. High levels of IL-6 correlated with the appearance of infectious complications in the post-traumatic course. These data indicate that the alterations in T-cell proliferation and IL-2 synthesis following major injury found in earlier studies are caused by different suppressor mechanisms. While T-cell proliferation is only decreased by extracellular components, IL-2 synthesis is suppressed mainly by an intracellular defect. The role of highly increased IL-6 levels and its effect on the immune response are so far unknown.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 0022-4804
e-ISSN 0022-4804
Quellenangaben Band: 48, Heft: 6, Seiten: 622-628 Artikelnummer: , Supplement: ,
Verlag Elsevier
Begutachtungsstatus Peer reviewed