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Cellular protein kinase C activity in asthma

I Vachier1, P Chanez, T Radeau

  • 1Clinique des Maladies Respiratoires, INSERM U 454, Hopital Arnaud de Villeneuve, France.

American Journal of Respiratory and Critical Care Medicine
|April 1, 1997
PubMed
Summary

Protein kinase C (PKC) activity is lower in neutrophils and macrophages of asthma patients, suggesting abnormal regulation contributes to inflammatory cell hyperreactivity in asthma.

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Area of Science:

  • Biochemistry
  • Immunology
  • Cell Biology

Background:

  • Protein kinase C (PKC) is crucial for cell signaling and implicated in inflammatory diseases.
  • Asthma involves activated inflammatory cells like alveolar macrophages (AM) and polymorphonuclear neutrophils (PMN), releasing increased reactive oxygen species.
  • PKC plays a significant role in the respiratory burst of human leukocytes.

Purpose of the Study:

  • To investigate and compare Protein Kinase C (PKC) activity in inflammatory cells from asthmatic and control subjects.
  • To determine if altered PKC activity correlates with the hyperreactivity observed in asthmatic inflammatory cells.

Main Methods:

  • PKC activity was measured in blood neutrophils and alveolar macrophages from 28 asthmatic and 16 control subjects.

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  • Total and membrane-bound PKC activity were assessed.
  • Neutrophil activity was also measured after stimulation with phorbol 12-myristate 13-acetate (PMA).

    • Main Results:

    • Total PKC activity was significantly lower in neutrophils from both stable and unstable asthmatic patients compared to controls.
    • Alveolar macrophages from asthmatic patients also showed significantly lower PKC activity than controls.
    • A higher percentage of membrane-bound PKC was observed in stable asthmatic patients' neutrophils and macrophages.
    • PMA stimulation caused a decrease in total PKC activity in neutrophils from both groups.

    Conclusions:

    • Asthma patients exhibit abnormal regulation of PKC activity in both blood neutrophils and alveolar macrophages.
    • These PKC dysregulations are consistent with the heightened functional activity of inflammatory cells seen in asthma.
    • Findings suggest a potential link between PKC signaling pathways and asthma pathophysiology.