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Microorganisms cause varying degrees of stimulation of superoxide (O2-) production (respiratory burst [RB]) in macrophages but in some cases apparently inhibit the RB induced in the same monolayers by a conventional stimulator. We have explored these differences. A mycobacterium model, the slowly multiplying mouse pathogen Mycobacterium microti, induced a modest RB in resident macrophage monolayers, compared with the substantial RB induced by opsonized zymosan (Zy). However, if the 1-h M. microti pulse immediately preceded the Zy assay (instead of being concurrent), the RB was consistently less than that elicited by the Zy alone. Cytochalasin (an inhibitor of phagocytosis) enhanced Zy-induced RB, supporting the view that the burst is cell surface mediated, but this agent apparently eliminated the inhibition of the Zy-induced RB caused by prior M. microti exposure, suggesting that this inhibition may have an intracellular origin. The inhibition described extended not only to another mycobacterium (Mycobacterium bovis BCG) but also to a previous application of Zy itself. The general implications for macrophage functions of these observations on timing and sites of initiation are briefly discussed.

infection and immunity

Stimulation or inhibition of the respiratory burst in cultured macrophages in a mycobacterium model: initial stimulation is followed by inhibition after phagocytosis