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Related Experiment Videos

TNF-alpha increases sensitivity to LPS in chronically catheterized rats.

M Goto1, L V Deriy, Y J Chen

  • 1Section of Neonatology, Department of Pediatrics, Rush Children's Hospital, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois 60612, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|May 18, 2001
PubMed
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Severe trauma increases tumor necrosis factor-alpha (TNF-alpha), making patients vulnerable to organ failure. TNF-alpha priming followed by bacterial toxin exposure significantly increases mortality and organ dysfunction markers.

Area of Science:

  • Immunology
  • Pathophysiology
  • Trauma Research

Background:

  • Severe trauma induces transient increases in serum tumor necrosis factor-alpha (TNF-alpha).
  • Elevated TNF-alpha levels predispose trauma patients to multisystem organ failure (MSOF).
  • Bacterial toxins, via infection or increased intestinal permeability, can trigger MSOF in trauma patients.

Purpose of the Study:

  • To investigate the role of TNF-alpha priming in the development of MSOF following bacterial toxin challenge.
  • To simulate the cytokine response seen in trauma patients using a rat model.

Main Methods:

  • Rats were primed with two doses of TNF-alpha (0.8 or 8.0 microg/kg).
  • After 48 hours, rats were challenged with lipopolysaccharide (LPS) at 10 or 1,000 microg/kg.

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  • Mortality, serum interferon-gamma (IFN-gamma), and blood lactate concentrations were measured.

    • Main Results:

    • TNF-alpha priming followed by high-dose LPS (1,000 microg/kg) significantly increased mortality, peak serum IFN-gamma, and blood lactate.
    • Lower-dose LPS (10 microg/kg) challenge increased IFN-gamma and lactate only in rats primed with the higher TNF-alpha dose (8.0 microg/kg).
    • Mortality was not increased with low-dose LPS challenge, even after TNF-alpha priming.

    Conclusions:

    • Both TNF-alpha release and subsequent bacterial toxin exposure are critical mediators in the progression from trauma to MSOF.
    • The study highlights a potential mechanism for increased susceptibility to organ failure after severe injury.