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*
Department of Surgery, Klinikum rechts der Isar, Technische Universität, München, Germany; and
Department of Medicine, Division of Immunology, Beth Israel Deaconess Medical Center, and
Department of Pathology, Harvard Medical School, Boston, MA 02215
Intra-abdominal infection in patients following major visceral
surgery is associated with high mortality. Using a macrophage depletion
technique, we demonstrate that in murine septic peritonitis, Kupffer
cells are a major source of systemic IL-10 levels. Kupffer
cell-depleted mice were highly susceptible to the lethal effects of
septic peritonitis and exhibited an increased bacterial load. Kupffer
cell-depleted mice were protected by the administration of an IL-10-Fc
fusion protein. Loss of Kupffer cell-derived IL-10 was associated with
a weak increase in serum IL-12 levels, whereas TNF, IL-1
, and IL-18
levels were not significantly elevated, suggesting that the loss of
Kupffer cell-derived IL-10 did not result in a toxic cytokine release
syndrome. Instead, loss of Kupffer cell-derived IL-10 was associated
with a reduced splenocyte production of IFN-
that is required for
immune protection in murine septic peritonitis. Therefore, the results
suggest that the protective function of IL-10 in septic peritonitis may
not be restricted to the anti-inflammatory activities of
IL-10.
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