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Departments of
*
Pathology and
Internal Medicine, Division of Pulmonary and Critical Care, University of Michigan Medical School, Ann Arbor, MI 48109
IL-13 has been shown to exert potent anti-inflammatory
properties. In this study, we elucidated the functional role of
endogenous IL-13 in a murine model of septic peritonitis induced by
cecal ligation and puncture (CLP). Initial studies demonstrated that
the level of IL-13 increased in tissues including liver, lung, and
kidney, whereas no considerable increase was found in either peritoneal
fluid or serum after CLP. Immunohistochemically, IL-13-positive cells
were Kupffer cells in liver, alveolar macrophages in lung, and
epithelial cells of urinary tubules in kidney. IL-13 blockade with
anti-IL-13 Abs significantly decreased the survival rate of mice
after CLP from 53% to 14% on day 7 compared with control. To
determine the potential mechanisms whereby IL-13 exerted a protective
role in this model, the effects of anti-IL-13 Abs on both local and
systemic inflammation were investigated. Administration of
anti-IL-13 Abs did not alter the leukocyte infiltration and
bacterial load in the peritoneum after CLP but dramatically increased
the neutrophil influx in tissues after CLP, an effect that was
accompanied by significant increases in the serum levels of aspartate
transaminase, alanine transaminase, blood urea nitrogen, and
creatinine. Tissue injury caused by IL-13 blockade was associated with
increases in mRNA and the protein levels of CXC chemokines macrophage
inflammatory protein-2 and KC as well as the CC chemokine macrophage
inflammatory protein-1
and the proinflammatory cytokine TNF-.
Collectively, these results suggest that endogenous IL-13 protected
mice from CLP-induced lethality by modulating inflammatory responses
via suppression of overzealous production of inflammatory
cytokines/chemokines in tissues.
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