 |
|
Interleukin-13 Effectively Down-regulates the Monocyte Inflammatory Potential During Traumatic Stress
Caroline Kim, MS;
Christian Schinkel, MD;
Dietmar Fuchs, MD;
Joseph Stadler, MD;
Alfred Walz, PhD;
Siegfried Zedler, DiplBiol;
Guido Henckel von Donnersmarck, MD;
Eugen Faist, MD
Arch Surg. 1995;130(12):1330-1336.
Abstract
| |
Objectives
To determine the potential of interleukin-13 (IL-13) to modify in vitro lipopolysaccharide-induced monocyte-macrophage (MO) activity in human cells from individuals who had sustained either major mechanical or burn injury and to investigate whether the effect of IL-13 is different on MOs that have been preactivated under traumatic stress than on monocytic cells from healthy volunteers.
Design
Peripheral MOs from 20 controls and 16 patients after major burn or mechanical trauma were separated on days 1, 3, 5, and 7 after injury and incubated with lipopolysaccharide (1 µg/mL) in the presence or absence of IL-13 (10 ng/mL) for 4 hours and for 20 hours. Thereafter, the following measures were determined from the culture supernatants: neopterin, nitric oxide, tumor necrosis factor  , IL-1β, IL-6, and IL-8.
Results
Ex vivo lipopolysaccharide-activated MOs, compared with control cells, displayed considerably enhanced inflammatory activity during the immediate posttraumatic course, with a substantial and consistent elevation of levels of tumor necrosis factor and IL-6. The addition of human recombinant IL-13 to the MO cultures resulted in an effective down-regulation of the synthesis of tumor necrosis factor , IL-1β, and IL-6 as well as IL-8, showing an average reduction of mediator production to two thirds of the value found in corresponding sole lipopolysaccharide-stimulated cultures. The impact of human recombinant IL-13 on control MOs was almost identical for IL-6 and IL-1β, slightly lower for IL-8, and nonexistent for tumor necrosis factor ,
Conclusion
From this study and preexisting findings, we conclude that, based on its biologic properties, IL-13 should be tested as a biologic response modifier for acute states of trauma-induced host defense deficiency.
(Arch Surg. 1995;130:1330-1336)
Author Affiliations
From the Department of Surgery, Ludwig-Maximilians-University, Klinikum Grosshadern, Munich, Germany (Ms Kim and Drs Schinkel, Zedler, and Faist); Institute of Medicine, Chemistry, and Biochemistry, University of Innsbruck (Austria) (Dr Fuchs); Department of Surgery, Technical University, Klinikum Rechts der Isar, Munich (Dr Stadler); Theodor-Kocher-Institute, University of Bern (Switzerland) (Dr Walz); and Community Hospital Munich-Bogenhausen, Munich (Dr Henckel von Donnersmarck).
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
|
