Monoclonal antibody to endotoxin core protects mice from Escherichia coli sepsis by a mechanism independent of tumor necrosis factor and interleukin-6

J Infect Dis. 1990 Aug;162(2):454-9. doi: 10.1093/infdis/162.2.454.

Abstract

To study the role of cytokines as mediators of endotoxin-induced shock, the serum levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6) were compared in mice receiving either a monoclonal antibody to endotoxin core (clone 20), an irrelevant monoclonal antibody (A1), or culture media (DMEM/FCS) alone before lethal challenge with live Escherichia coli O111:B4. Clone 20 given 1.5 h before the bacterial challenge protected mice from death (mortality at 48 h 3% vs. 87%, P less than .001). The pattern of IL-6 release was indistinguishable in clone 20 recipients and controls: The area under the curve (AUC) for 5 h was 1.22 +/- 0.07 x 10(6), 1.03 +/- 0.17 x 10(6), and 1.22 +/- 0.07 x 10(6) units/ml for clone 20, A1, and DMEM/FCS, respectively. Similarly, the timing and extent of TNF release in the serum was virtually identical in clone 20 recipients that survived and control animals that died. AUC for 5 h was 30.8 +/- 4.0 x 10(3), 28.1 +/- 1.1 x 10(3), and 30.4 +/- 4.7 x 10(3) ng/ml in clone 20, A1, and DMEM/FCS recipients, respectively. Thus, TNF and IL-6 appear insufficient to cause death in this model of experimental gram-negative shock.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / therapeutic use*
  • Disease Models, Animal
  • Endotoxins / immunology*
  • Escherichia coli Infections / etiology
  • Escherichia coli Infections / prevention & control*
  • Immunization, Passive
  • Interleukin-6 / analysis*
  • Interleukin-6 / biosynthesis
  • Male
  • Mice
  • Shock, Septic / etiology
  • Shock, Septic / prevention & control
  • Tumor Necrosis Factor-alpha / analysis*
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Antibodies, Monoclonal
  • Endotoxins
  • Interleukin-6
  • Tumor Necrosis Factor-alpha