SUMMARY: When ingested by mouse peritoneal macrophage monolayers, live caused a sustained increase in monolayer cyclic AMP content and fusion of lysosomes with the bacterium-containing phagosomes was impaired. Ingested live BCG caused a transient increase in cyclic AMP and the defect in phagolysosome formation was less pronounced. Dead mycobacteria and live neither enhanced monolayer cyclic AMP content nor inhibited phagolysosome formation. and BCG exceeded in cyclic AMP-synthesizing activity but the question of whether bacterial cyclic AMP contributed substantially to the increments in infected macrophages was not resolved. Antibody-coated BCG retained the ability to synthesize cyclic AMP and to enhance monolayer cyclic AMP but lost the ability to inhibit phagolysosome formation in macrophages. The observations are discussed in terms of possible control of phagolysosome formation by cyclic nucleotides.


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