Interleukin-13 effectively down-regulates the monocyte inflammatory potential during traumatic stress
C. Kim, C. Schinkel, D. Fuchs, J. Stadler, A. Walz, S. Zedler, G. H. von Donnersmarck and E. Faist
Department of Surgery, Ludwig-Maximilians-University, Klinikum Grosshadern, Munich, Germany.
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
microgram/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
alpha, IL-1 beta, 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 alpha 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 alpha, IL-1 beta, 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-1 beta, slightly lower for IL-8, and nonexistent
for tumor necrosis factor alpha. 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.
