期刊
BURNS
卷 37, 期 7, 页码 1208-1215出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.burns.2011.04.010
关键词
Phagocytosis; Reactive oxygen species; Post-burn infection; CD68(+) Kupffer cells
资金
- Japan Ministry of Defense
- Grants-in-Aid for Scientific Research [22650154, 21300237] Funding Source: KAKEN
We recently demonstrated that IL-18 injections following burn restored IFN-gamma production and increased mouse survival after bacterial infection. However, it has yet to be fully elucidated how the IL-18 therapy affects the function of phagocytic cells. We investigated the effect of IL-18 therapy on function and interaction of Kupffer cells and NK cells in burned mice. C57BL/6 mice received a 20% full-thickness burn, followed by multiple injections with IL-18. Although burn-injured mice had decreased expression of IL-18 receptors on the NM/NKT cells 5 days after injury, multiple IL-18 injections restored this expression. IL-18 treatment also augmented Kupffer cell phagocytosis. Although burn decreased the number of CD68(+) Kupffer cells with phagocytic activity, IL-18 treatment partially restored their proportion, and augmented phagocytosis-induced ROS production in CD68(+) Kupffer cells after the injection of heat-killed Escherichia coli. Consistently, IL-18 restored the impaired E. coli killing activity of Kupffer cells of burn-injured mice. Such Kupffer cell activation by IL-18 was abrogated by the deletion of NK cells or IFN-gamma. In conclusion, IL-18 therapy in burn-injured mice enhanced function of CD68(+) Kupffer cells via the activation of liver NM cells and augmentation of their IFN-gamma production, thereby improving survival after E. coli infection. Crown Copyright (C) 2011 Published by Elsevier Ltd and ISBI. All rights reserved.
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