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and TNF-
production
Departments of 1 Medicine and 3 Surgery, University of Colorado Health Sciences Center, Denver, Colorado 80206; 2 Division of Clinical Pharmacology, Medizinische Klinik Innenstadt, Klinikum of the Ludwig-Maximilians-University Munich, 80336 Munich; and 4 Institute of Pathology, University of Mainz, 55131 Mainz, Germany
Interleukin (IL)-18,
initially described as interferon (IFN)-
-inducing factor, is
expressed in the inflamed mucosa of patients with Crohn's disease. To
investigate the role of IL-18 in intestinal inflammation, the effect of
neutralizing antimurine IL-18 antiserum in dextran sulfate sodium
(DSS)-induced colitis in BALB/c and C57BL/6 mice was examined. During a
dose response of DSS, levels of colonic IL-18 increased parallel with
clinical worsening. With the use of confocal laser microscopy, the
increased IL-18 was localized to the intestinal epithelial layer.
Anti-IL-18 treatment resulted in a dose-dependent reduction of the
severity of colitis in both BALB/c and C57BL/6 mice. Colon shortening
following DSS-induced colitis was partially prevented in the treatment
groups. In the colon tissue homogenates, IFN- concentrations were
lower in the anti-IL-18-treated DSS-fed mice compared with untreated
DSS-fed mice. This suppressive effect of anti-IL-18 administered in
vivo was also observed on spontaneous tumor necrosis factor-
, IL-18, and IFN- production from ex vivo colon organ cultures. The
stimulation of lamina propria mononuclear cells by IL-18 and IL-12
resulted in a synergistic increase in IFN- synthesis. These findings
suggest that IL-18 is a pivotal mediator in experimental colitis.
inflammation; cytokines; antibodies; in vivo animal models
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