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The Pattern of Interleukin-1 (IL-1) and Its Modulating Agents IL-1 Receptor Antagonist and IL-1 Soluble Receptor Type II in Acute Meningococcal Infections
Marcel van Deuren,
Johanna van der Ven-Jongekrijg,
Edouard Vannier,
Roelof van Dalen,
Gerard Pesman,
Anton K.M. Bartelink,
Charles A. Dinarello, and
Jos W.M. van der Meer
From the Departments of Internal Medicine, Intensive Care, Laboratory of Endocrinology and Reproduction, University Hospital Nijmegen, Nijmegen; the Department of Internal Medicine, Eemland Hospital Amersfoort, Amersfoort, The Netherlands; New England Medical Center, Boston, MA; and the Division of Infectious Diseases, University of Colorado Health Science Center, Denver.
Interleukin-1 (IL-1) is considered an important mediator in the pathogenesis of septic shock or bacterial meningitis. Its activity is specifically modulated by IL-1 receptor antagonist (IL-1Ra) and IL-1 soluble receptor type II (IL-1sRII). We now describe the time-course of IL-1 and these modulating agents in 59 patients with acute meningococcal infections, the prototype human disease of acute endotoxin exposure. Plasma IL-1 was increased only in severe shock and normalized within 12 to 24 hours, indicating that patients were admitted in an early stage of cytokine activation. Increased IL-1 values in cerebrospinal fluid (CSF ) were confined to patients with meningitis. Plasma IL-1Ra was elevated in both shock and nonshock patients, extremely high values being measured in severe shock. High concentrations of IL-1Ra in CSF were found in meningitis. Plasma IL-1Ra peaked shortly after IL-1 and decreased steeply in 1 to 2 days, followed by sustained moderately elevated levels in shock patients. Interestingly, IL-1sRII showed a completely different pattern. At admission, both nonshock and shock patients manifested a similar moderate increase of plasma IL-1sRII. However, during recovery plasma IL-1sRII further increased reaching maximal concentrations 3 to 5 days after admission, 1 to 2 days after normalization of IL-1Ra. In shock patients this increase was more prominent than in nonshock patients. It is hypothesized that this increase in plasma IL-1sRII can be explained by a synergistic effect of dexamethasone and endotoxin. A second interesting observation was that, unlike the pattern in plasma, IL-1sRII levels in CSF paralleled those of IL-1 and IL-1Ra. This suggests different modulation of IL-1 activity in the subarachnoid space and the plasma compartment. We conclude that: (1) During the early stage of meningococcal infections IL-1Ra modulates IL-1 activity, whereas during recovery IL-1sRII may be more important. (2) Modulation in CSF and in the plasma compartment are differentially regulated.
Blood, Vol. 90 No. 3 (August 1), 1997:
pp. 1101-1108
© 1997 by The American Society of Hematology.
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