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Production from Liver Mononuclear Cells of Mice in Burn Injury As Well As in Postburn Bacterial Infection Models and the Therapeutic Effect of IL-18
* Division of Basic Traumatology, National Defense Medical College Research Institute, and Departments of
Surgery 1 and
Microbiology, National Defense Medical College, Namiki, Tokorozawa, Japan; and
First Department of Surgery, Tokyo Medical and Dental University, Tokyo, Japan
Hosts after severe burn injury are known to have a defect in the
Th1 immune response and are susceptible to bacterial infections. We
herein show that liver NK cells are potent IFN-
producers early
after burn injury. However, when mice were injected with LPS 24 h
after burn injury, IFN- production from liver mononuclear cells
(MNC; which we previously showed to be NK cells) was suppressed, and
the serum IFN- concentration did not increase, while serum IL-10
conversely increased compared with control mice. Interestingly, a
single injection of IL-18 simultaneously with LPS greatly restored the
serum IFN- concentration in mice with burn injury and also increased
IFN- production from liver MNC. Nevertheless, a single IL-18
injection into mice simultaneously with LPS was no longer effective in
the restoration of serum IFN- and IFN- production from the liver
MNC at 7 days after burn injury, when mice were considered to be the
most immunocompromised. However, IL-18 injections into mice on
alternate days beginning 1 day after burn injury strongly up-regulated
LPS-induced serum IFN- levels and IFN- production from liver and
spleen MNC of mice 7 days after burn injury and down-regulated serum
IL-10. Furthermore, similar IL-18 therapy up-regulated serum IFN-
levels in mice with experimental bacterial peritonitis 7 days after
burn injury and greatly decreased mouse mortality. Thus, IL-18 therapy
restores the Th1 response and may decrease the susceptibility to
bacterial infection in mice with burn injury.
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