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Related Experiment Videos

Corticosteroid-resistant chronic asthma and monocyte complement receptors

A B Kay, P Diaz, J Carmicheal

    Clinical and Experimental Immunology
    |June 1, 1981
    PubMed
    Summary

    Corticosteroids decrease monocyte complement receptors (MCR) and their enhancement (CRE) in asthma patients who respond to treatment. Resistant asthmatics may have a defect in complement receptor expression.

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    Area of Science:

    • Immunology
    • Pulmonology

    Background:

    • Chronic asthma involves complex immune dysregulation.
    • Corticosteroids are a cornerstone therapy, but response varies significantly.
    • Monocyte complement receptors (MCR) and their enhancement (CRE) play roles in inflammation.

    Purpose of the Study:

    • To investigate MCR and CRE levels in corticosteroid-resistant versus responsive chronic asthmatics.
    • To determine the effect of systemic corticosteroids on MCR and CRE in asthma.

    Main Methods:

    • Measurement of monocyte complement receptors (MCR) and casein-induced enhancement of MCR (CRE).
    • Comparison of MCR and CRE in newly-diagnosed, corticosteroid-responsive, and corticosteroid-resistant asthmatic patients.
    • Assessment of MCR and CRE before and after prednisolone treatment, and during withdrawal.

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    Main Results:

    • In responsive asthmatics, prednisolone significantly decreased MCR and CRE percentages.
    • MCR and CRE levels returned to baseline upon prednisolone withdrawal.
    • Corticosteroid-resistant asthmatics showed no significant decrease in MCR and CRE while on prednisolone compared to responsive asthmatics.
    • No significant difference in MCR and CRE was observed between non-responders on prednisolone and those on other therapies.

    Conclusions:

    • Systemic corticosteroids reduce MCR and CRE in asthma patients who respond to treatment.
    • Corticosteroid-resistant chronic asthmatics may possess a defect in monocyte complement receptor expression or mobilization.
    • These findings suggest a potential mechanism for corticosteroid resistance in asthma.