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Related Experiment Videos

Nitric oxide and asthmatic inflammation

P J Barnes1, F Y Liew

  • 1Dept of Thoracic Medicine, National Heart and Lung Institute, London, UK.

Immunology Today
|March 1, 1995
PubMed
Summary

Nitric oxide (NO) from airway cells may worsen asthma by inhibiting T helper 1 (Th1) cells. Targeting inducible nitric oxide synthase (iNOS) could be a new treatment for asthma and allergies.

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Area of Science:

  • Immunology
  • Respiratory Medicine
  • Molecular Biology

Background:

  • Asthmatic patients exhibit elevated inducible nitric oxide synthase (iNOS) expression in airway epithelial cells.
  • Increased nitric oxide (NO) levels are detected in the exhaled air of individuals with asthma.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) in amplifying and perpetuating asthmatic inflammation.
  • To explore the potential of inducible nitric oxide synthase (iNOS) inhibitors as a novel therapeutic strategy for asthma and allergic diseases.

Main Methods:

  • The study discusses the proposed mechanism involving NO derived from airway epithelial cells.
  • It examines the impact of NO on T helper cell populations and cytokine production.

Main Results:

  • Nitric oxide (NO) may inhibit T helper 1 (Th1) cells and interferon gamma (IFN-gamma) production.
  • This inhibition leads to an increase in T helper 2 (Th2) cells, interleukin 4 (IL-4), and interleukin 5 (IL-5), promoting airway inflammation and eosinophil recruitment.

Conclusions:

  • The described mechanism, while part of normal defense, appears inappropriately activated in asthma.
  • Specific inhibitors of inducible nitric oxide synthase (iNOS) represent a promising novel therapeutic approach for asthma and other allergic conditions.

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