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(Journal of Leukocyte Biology. 2002;72:643-649.)
© 2002 by Society for Leukocyte Biology

High circulating levels of the IL-1 type II decoy receptor in critically ill patients with sepsis: association of high decoy receptor levels with glucocorticoid administration

Beat Müller*, Giuseppe Peri{dagger}, Andrea Doni{dagger}, André P. Perruchoud*, Regine Landmann{ddagger}, Fabio Pasqualini{dagger} and Alberto Mantovani{dagger},§

Departments of
* Internal Medicine and
{ddagger} Research, University Hospitals, Basel, Switzerland;
{dagger} Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy; and
§ Centro di Eccellenza IDET, Department of Pathology, University of Milan, Italy

Correspondence: Prof. Alberto Mantovani, Istituto di Ricerche Farmacologiche "Mario Negri", Via Eritrea 62, 20157 Milan, Italy. E-mail: Mantovani{at}marionegri.it

The objective of this study was to evaluate whether the interleukin (IL)-1 decoy receptor (R), a negative pathway of regulation of IL-1, is correlated with severity of infection in critically ill patients and reflects the activation of anti-inflammatory pathways by glucocorticoid hormones. Plasma samples were obtained from 101 consecutive, critically ill patients admitted to the intensive care unit with different severities of microbial infection, as defined by standardized criteria. Here, we report that the IL-1 type II decoy R(II) is elevated in critically ill patients, especially in severe, systemic infection and culture-positive infections. In patients with a marked systemic inflammatory response syndrome 4, a pronounced, sepsis-induced further increase of circulating IL-1 decoy RII levels was evident. Thirty-six patients treated with glucocorticoid hormones had significantly higher levels of IL-1 decoy RII, but lower IL-6 and C-reactive protein, than 67 untreated subjects. The usefulness of IL-1RII, in particular as a potential marker for the activation of anti-inflammatory pathways or for responsiveness to anti-inflammatory agents such as glucocorticoid hormones, deserves further analysis.

Key Words: microbial infection • severe sepsis • glucocorticoid hormones • cytokines




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