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Inducible nitric oxide synthase gene expression and enzyme activity correlate with disease activity in murine

A H Cross1, R M Keeling, S Goorha

  • 1Department of Neurology and Neurosurgery, Washington University School of Medicine, St. Louis, MO 63110, USA. crossa@neuro.wustl.edu

Insights

This study shows increased inducible nitric oxide synthase (iNOS) mRNA and activity in the spinal cord during experimental allergic encephalomyelitis (EAE) in mice. These findings suggest a role for excess nitric oxide (NO) in this autoimmune disease model.

Area of Science:

  • Neuroimmunology
  • Molecular Biology
  • Pathology

Background:

  • Experimental allergic encephalomyelitis (EAE) is a mouse model for central nervous system (CNS) autoimmune diseases.
  • Inducible nitric oxide synthase (iNOS) produces nitric oxide (NO), a molecule implicated in various physiological and pathological processes.

Purpose of the Study:

  • To investigate the expression and activity of iNOS in the spinal cord during EAE.
  • To determine the potential role of iNOS-derived NO in the pathogenesis of EAE.

Main Methods:

  • Messenger RNA (mRNA) encoding iNOS was quantified using competitive reverse transcriptase polymerase chain reaction (cRT-PCR) and ribonuclease protection assays.
  • Functional iNOS activity was assessed by measuring calcium-independent citrulline production.

Main Results:

  • iNOS mRNA levels were significantly elevated (10-20 fold) in the spinal cords of mice with acute EAE compared to controls.
  • Functional iNOS activity was also markedly increased in spinal cords during active EAE.

Conclusions:

  • The heightened expression and activity of iNOS in EAE spinal cords correlate with active disease.
  • These results support a pathogenic role for excess nitric oxide (NO) in this model of CNS autoimmunity.

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