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The anticomplementary effect of kidney tissue; its association with ammonia production

P B BEESON, D ROWLEY

    The Journal of Experimental Medicine
    |November 1, 1959
    PubMed

    Insights

    Kidney tissue uniquely hinders serum’s ability to fight coliform bacteria due to potent anticomplementary activity. This finding may explain kidney vulnerability to infections, particularly those involving complement and antibody-mediated bacterial destruction.

    Area of Science:

    • Immunology
    • Nephrology
    • Microbiology

    Background:

    • Kidney susceptibility to coliform bacterial infections is a significant clinical problem.
    • Normal serum's complement system plays a crucial role in bacterial clearance.
    • The kidney's unique role in immune defense against bacterial pathogens requires further elucidation.

    Purpose of the Study:

    • To investigate the mechanisms underlying the kidney's peculiar susceptibility to coliform bacterial infections.
    • To determine if kidney tissue possesses unique properties that affect serum's bactericidal activity.
    • To identify the specific component of the complement system involved and its interaction with kidney tissue.

    Main Methods:

    • Comparative analysis of anticomplementary activity in kidney tissue versus other organs.
    • Characterization of the heat-lability, dialyzability, and particulate nature of the active principle.
    • Investigation of the specific complement component affected by kidney tissue.
    • Examination of factors influencing complement inactivation, such as ammonia formation, phosphate, and glutamine.

    Main Results:

    • Kidney tissue exhibits 5-15 times greater anticomplementary activity than other organs, inhibiting serum's ability to destroy coliform bacteria.
    • Complement inactivation by kidney tissue is a chemical reaction involving a heat-labile, non-dialyzable factor associated with tissue particles.
    • The fourth component of complement (C4) is specifically affected, showing susceptibility to ammonia-like injury.
    • Phosphate and glutamine enhance complement inactivation by kidney homogenates, similar to ammonia formation conditions.

    Conclusions:

    • Kidney tissue possesses a potent anticomplementary activity that impairs bacterial killing by normal serum.
    • This anticomplementary effect, particularly involving the C4 component, may contribute to the kidney's vulnerability to specific bacterial infections.
    • The findings suggest a novel mechanism explaining kidney infection susceptibility, especially for bacteria targeted by complement and antibody-mediated immunity.
    Keywords:
    AMMONIA/metabolismKIDNEY/physiology

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