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Complement levels in pneumococcal pneumonia.

J D Coonrod, B Rylko-Bauer

    Infection and Immunity
    |October 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

    Pneumococcal pneumonia selectively depresses the alternate complement pathway, especially with bacteremia. This pathway

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    Area of Science:

    • Immunology
    • Infectious Diseases
    • Complement System Biology

    Background:

    • Pneumococcal pneumonia is a significant cause of morbidity and mortality.
    • The complement system plays a crucial role in host defense against bacterial infections.
    • The alternate complement pathway is a key component of innate immunity.

    Purpose of the Study:

    • To investigate the levels and functional activity of complement proteins in patients with pneumococcal pneumonia.
    • To determine the specific involvement of the alternate complement pathway in this infection.
    • To assess the impact of bacteremia on complement activation.

    Main Methods:

    • Assessed complement protein levels (C3, properdin, factor B, C4, C1q) in patient sera.
    • Measured functional activity of the alternate complement pathway.

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  • Compared complement levels between patients with and without bacteremia.
  • Analyzed complement levels during acute infection and convalescence.

    • Main Results:

    • Significantly lower mean levels of C3 and properdin, and reduced alternate pathway activity were observed in acute pneumococcal pneumonia.
    • Classical pathway components remained normal.
    • Patients with bacteremia showed more severe depression of properdin and factor B.
    • Properdin levels and alternate pathway activity remained low during convalescence in bacteremic patients.

    Conclusions:

    • Pneumococcal pneumonia causes selective depression of the alternate complement pathway.
    • Bacteremia exacerbates this depression.
    • The findings support the role of the alternate complement pathway in defending against pneumococcal infections.