Gut mucosal homeostasis and cellular mediators after severe thermal trauma and the effect of insulin-like growth factor-I in combination with insulin-like growth factor binding protein-3

Marc G. Jeschke, Ullrich Bolder, Dai H. Chung, Rene Przkora, Ulla Mueller, James C. Thompson, Steven Wolf, David Herndon

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Increased small bowel epithelial cell apoptosis and decreased cell proliferation lead to impairment of gut mucosal integrity and function after thermal injury. Impairment of gut integrity is associated with increased bacterial translocation and incidence of sepsis. The purpose of this study was to determine whether IGF-I/IGF binding protein (IGFBP)-3 can improve small bowel homeostasis after injury and by which cellular mechanisms these changes occur and to identify changes in apoptosis-related genes after burn and the effect of bile acid on small bowel epithelial cell apoptosis after burn. Rats sustained a thermal injury and received saline or the IGF-I/IGFBP-3 complex. Serum and small intestine were taken at 1, 2, 5, and 7 d after injury and serum inflammatory cytokines and mucosal apoptosis, proliferation, villous morphology, and apoptotic and proliferative mediators were measured. Apoptosis-related gene expression and the bile acid pool were determined in separate experiments up to 6 h after burn. Gut epithelial cell apoptosis as well as apoptosis-related genes were increased after the thermal injury, whereas bile acid secretion was significantly decreased (P < 0.05). IGF-I/IGFBP-3 significantly improved villous height and cells per villous by decreasing small bowel epithelial cell apoptosis and increasing proliferation (P < 0.05). Decreased apoptosis was associated with decreased Fas, Fas-ligand, and TNF when compared with saline (P < 0.05). A severe thermal injury caused an up-regulation of apoptosis and apoptosis-related genes and down-regulation of bile acid secretion. IGF-I/IGFBP-3 decreases small bowel epithelial cell apoptosis through down-regulation of the Fas pathway, which improves gut mucosal integrity after a severe thermal injury.

Original languageEnglish (US)
Pages (from-to)354-362
Number of pages9
JournalEndocrinology
Volume148
Issue number1
DOIs
StatePublished - 2007

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Insulin-Like Growth Factor Binding Protein 3
Insulin-Like Growth Factor I
Homeostasis
Hot Temperature
Apoptosis
Wounds and Injuries
Bile Acids and Salts
Epithelial Cells
Down-Regulation
Genes
Bacterial Translocation
Fas Ligand Protein
Serum
Small Intestine
Sepsis
Up-Regulation

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Gut mucosal homeostasis and cellular mediators after severe thermal trauma and the effect of insulin-like growth factor-I in combination with insulin-like growth factor binding protein-3. / Jeschke, Marc G.; Bolder, Ullrich; Chung, Dai H.; Przkora, Rene; Mueller, Ulla; Thompson, James C.; Wolf, Steven; Herndon, David.

In: Endocrinology, Vol. 148, No. 1, 2007, p. 354-362.

Research output: Contribution to journalArticle

Jeschke, Marc G. ; Bolder, Ullrich ; Chung, Dai H. ; Przkora, Rene ; Mueller, Ulla ; Thompson, James C. ; Wolf, Steven ; Herndon, David. / Gut mucosal homeostasis and cellular mediators after severe thermal trauma and the effect of insulin-like growth factor-I in combination with insulin-like growth factor binding protein-3. In: Endocrinology. 2007 ; Vol. 148, No. 1. pp. 354-362.
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