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Anthrax toxin blocks priming of neutrophils by lipopolysaccharide and by muramyl dipeptide

G G Wright, G L Mandell

    The Journal of Experimental Medicine
    |November 1, 1986
    PubMed

    Insights

    Anthrax toxin components inhibit the priming of human neutrophils (PMN) by bacterial products like LPS and MDP. This inhibition reduces superoxide anion release, impairing antimicrobial effects.

    Area of Science:

    • Immunology
    • Microbiology
    • Toxicology

    Background:

    • Human polymorphonuclear neutrophils (PMN) are crucial for innate immunity.
    • Bacterial products like lipopolysaccharide (LPS) and muramyl dipeptide (MDP) can prime PMN, enhancing their antimicrobial functions.
    • Anthrax toxin is a tripartite toxin composed of protective antigen (PA), edema factor (EF), and lethal factor (LF).

    Purpose of the Study:

    • To investigate the effects of anthrax toxin components (PA, EF, LF) on the priming of human PMN.
    • To determine if anthrax toxin inhibits the enhanced superoxide anion release from primed PMN.
    • To understand the implications of anthrax toxin's effect on PMN antimicrobial activity.

    Main Methods:

    • Human PMN were pretreated with purified anthrax toxin components (PA, EF, LF) or combinations thereof.
    • PMN priming was induced using LPS or MDP.
    • Superoxide anion (O-2) release was measured after stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbol myristate acetate (PMA).

    Main Results:

    • Anthrax toxin components PA plus EF or PA plus LF significantly inhibited LPS- or MDP-induced PMN priming, reducing O-2 release by up to 90%.
    • Single anthrax toxin components did not inhibit priming.
    • Inhibition was less pronounced if PMN were primed before toxin exposure.
    • Anthrax toxin did not affect O-2 release stimulated by PMA.

    Conclusions:

    • Anthrax toxin inhibits the priming of human PMN by bacterial products.
    • This inhibition impairs the full expression of PMN antimicrobial effects.
    • The findings suggest a mechanism by which anthrax toxin may compromise host defense.

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