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Interactions between Mycoplasma pneumoniae and guinea pig complement.

W Bredt, D Bitter-Suermann

    Infection and Immunity
    |March 1, 1975
    PubMed
    Summary
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    Guinea pig serum (GPS) exhibits toxicity towards Mycoplasma pneumoniae, mediated by the complement system. This interaction, involving both classical and alternative complement pathways, can lead to cell death or damage.

    Area of Science:

    • Immunology
    • Microbiology
    • Complement System Research

    Background:

    • Mycoplasma pneumoniae infections can cause significant respiratory illness.
    • The role of serum components, particularly complement, in host defense against bacteria is well-established.
    • The specific mechanisms by which serum exerts toxic effects on Mycoplasma pneumoniae are not fully elucidated.

    Purpose of the Study:

    • To investigate the "toxic" effects of guinea pig serum (GPS) on Mycoplasma pneumoniae cells.
    • To identify the specific components within GPS responsible for these cytotoxic activities.
    • To elucidate the pathways of complement activation involved in the interaction with Mycoplasma pneumoniae.

    Main Methods:

    • Testing the "toxic" effects of GPS on Mycoplasma pneumoniae, measuring cell rounding and killing.

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  • Heat inactivation of GPS to assess the role of heat-labile components.
  • Assessing the requirement for divalent cations (Ca2+, Mg2+) and complement components (C1, C4, C6, C3, Properdin factor D) using depleted or deficient sera and specific antisera.
  • Utilizing immune adherence to detect C3b deposition and immune fluorescence to check for antibodies.

    • Main Results:

    • Both killing and rounding activities of GPS on Mycoplasma pneumoniae were heat-labile.
    • Killing required both Ca2+ and Mg2+, while rounding required only Mg2+.
    • Defects in early complement components (C1, C4, C6) significantly impaired killing but only slightly affected rounding.
    • Anti-C3 antiserum blocked both activities, and properdin factor D was necessary for rounding via the alternative pathway.
    • C3b deposition was observed on Mycoplasma pneumoniae cells after GPS treatment, indicating complement activation.
    • No specific antibodies against Mycoplasma pneumoniae were detected in the GPS.

    Conclusions:

    • Complement is the primary toxic factor in GPS responsible for Mycoplasma pneumoniae cell damage.
    • Mycoplasma pneumoniae can activate both the classical and alternative complement pathways.
    • The interaction with complement may lead to cell death or damage, potentially contributing to disease pathogenesis even without specific antibodies.