Abstract

Recent reports have suggested that interactions between the lipopolysaccharide receptor CD14 and heat shock proteins (Hsps) play roles in proinflammatory responses. The involvement of glucose-regulated protein 78 (Grp78), a member of Hsp70 family, and CD14 in signaling events activated in the liver and lungs of mice after burn injury was investigated. Differential induction of Grp78 in the liver of CD14 knockout (KO) mice after 18% total body surface area burn was associated with a transient down-regulation of serum glucose level at day 1 after injury. Subsequent studies revealed that the liver of both CD14 KO and wild-type control mice had a significant induction of Grp78 mRNA at day 1 after injury, while the level of induction was greater in CD14 KO mice. In contrast, in the lungs, there was an up-regulation of Grp78 mRNA only in CD14 KO mice at day 1 after injury. Interestingly, both the liver and the lungs had no apparent changes in Grp78 protein expression after injury. These data demonstrate CD14-dependent and tissue-specific regulation of the Grp78 expression after burn injury. They also suggest potential activation of a CD14-independent signaling pathway involving Grp78 in distant organs after injury.

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