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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
The present study addressed the role of IL-12 in a murine model of
septic peritonitis, induced by cecal ligation and puncture (CLP).
Although CLP surgery induced IL-12 production at 6 and 24 h after
surgery, IL-12 immunoneutralization was clearly deleterious in this
model: 54% of CLP mice receiving preimmune serum survived, whereas
mice administered IL-12 antisera prior to CLP experienced a 25%
survival rate. IL-12 immunoneutralization not only led to increased
mortality, but also appeared to promote a shift away from IL-12 and
IFN-
, in favor of IL-10. This cytokine shift corresponded to changes
in bacterial load, as CLP mice receiving IL-12 antiserum yielded more
CFUs from the peritoneal cavity at 24 h after CLP. To address the
role of bacterial infection in IL-12 antiserum-induced mortality
following CLP, antibiotics were administered for 4 days after surgery.
Despite regular antibiotic administration, IL-12 immunoneutralization
still reduced survival in CLP mice. Furthermore, histology of the ceca
revealed that mice administered IL-12 antisera failed to show typical
organization of the damaged cecum wall. Accordingly, Gram staining
revealed bacteria within peritoneal fluids from these mice, while
peritoneal fluids from CLP mice that received preimmune serum and
antibiotics were free of bacteria. Altogether, these data suggested
multiple important roles for IL-12 in the evolution of murine septic
peritonitis.
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