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Neutral endopeptidase modulates septic shock

B Lu1, N P Gerard, L F Kolakowski

  • 1The Ina Sue Perimutter Laboratory, Boston, Massachusetts 02115, USA.

Annals of the New York Academy of Sciences
|March 22, 1996
PubMed
Summary
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Neutral endopeptidase (NEP) plays a protective role in endotoxin shock. Mice lacking NEP show increased sensitivity to endotoxin, indicating NEP

Area of Science:

  • Biochemistry
  • Immunology
  • Molecular Biology

Background:

  • Neutral endopeptidase (NEP), also known as CD10, is a cell-surface metalloproteinase.
  • NEP degrades oligopeptide agonists, terminating signaling pathways.
  • Its role in septic shock was previously unclear.

Purpose of the Study:

  • To investigate the role of NEP in endotoxin shock.
  • To determine the effect of NEP deficiency on lethality and mediator sensitivity.

Main Methods:

  • Targeted disruption of the NEP gene in mice.
  • Administration of endotoxin to wild-type and NEP-deficient mice.
  • Assessment of survival rates and sensitivity to TNF and IL-1.

Main Results:

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  • NEP-deficient mice exhibited enhanced lethality to endotoxin shock.
  • A gene-dosage effect was observed, with higher NEP deficiency correlating with increased lethality.
  • NEP-deficient animals showed increased sensitivity to tumor necrosis factor (TNF) and interleukin-1 (IL-1).

Conclusions:

  • NEP plays a crucial protective role in septic shock.
  • NEP's protective mechanism appears to act downstream of TNF and IL-1 release.
  • Targeting NEP may offer a therapeutic strategy for septic shock.