Increased extra domain-A containing fibronectin and hepatic dysfunction during septic response: an in vivo and in vitro study

Shock. 2000 Jun;13(6):492-6. doi: 10.1097/00024382-200006000-00012.

Abstract

A massive inflammatory reaction resulting from systemic cytokine release is the common pathway underlying sepsis or multiple organ dysfunction. The role of extra domain sequence A-containing fibronectin (EDA+FN) formation during the septic response is not known. The present study investigates the role of EDA+FN during the septic response under in vitro and in vivo conditions. The direct effects of interleukin-1, interleukin-6, and tumor necrosis factor-alpha on EDA+FN production were evaluated in primary cultured human hepatocytes and fibroblasts. Serial plasma EDA+FN levels were measured using an enzyme-linked immunosorbent assay in 24 patients who developed postoperative sepsis following general abdominal surgery of which there were 17 survivors and 7 non-survivors. EDA+FN secretion was significantly increased in cultured hepatocytes but not fibroblasts at 24 and 48 h following exposure to IL-1 compared to controls. In the clinical setting plasma EDA+FN levels in non-survivors were significantly higher than in survivors. Moreover, the EDA+FN levels were correlated closely with liver function tests. EDA+FN levels may represent a specific marker of vascular injury or systemic inflammatory response syndrome that is associated with an adverse clinical outcome.

Publication types

  • Comparative Study

MeSH terms

  • APACHE
  • Abdomen / surgery
  • Aged
  • Biomarkers
  • Cells, Cultured
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Fibronectins / blood*
  • Fibronectins / chemistry
  • Fibronectins / genetics
  • Humans
  • Interleukin-1 / pharmacology
  • Interleukin-6 / pharmacology
  • Liver / cytology
  • Liver / metabolism*
  • Liver Function Tests
  • Male
  • Middle Aged
  • Multiple Organ Failure / metabolism
  • Multiple Organ Failure / mortality
  • Postoperative Complications / metabolism*
  • Postoperative Complications / mortality
  • Protein Isoforms / blood*
  • Protein Isoforms / chemistry
  • Protein Isoforms / genetics
  • Protein Structure, Tertiary
  • Recombinant Fusion Proteins / pharmacology
  • Systemic Inflammatory Response Syndrome / metabolism*
  • Systemic Inflammatory Response Syndrome / mortality
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Biomarkers
  • Fibronectins
  • Interleukin-1
  • Interleukin-6
  • Protein Isoforms
  • Recombinant Fusion Proteins
  • Tumor Necrosis Factor-alpha