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Mycobacterium microti may protect itself from intracellular destruction by releasing cyclic AMP into phagosomes


PATHOGENIC mycobacteria are able to survive and multiply within macrophages. How they do this is not known, but recent quantitative electron microscope surveys of intracellular events in macrophages infected in vitro with either Mycobacterium tuberculosis or M. microti revealed a lack of discharge of lysosomes into phagosomes containing live bacilli, whereas dead bacilli were associated with discharged lysosomal contents within phagolysosomes1,2. Possibly the living bacteria produce a factor which inhibits fusion between phagosomal and lysosomal membranes and thereby prevent the discharge of putatively bactericidal lysosomal contents into the bacterial environment. Since high intracellular levels of cyclic adenosine 3′,5′-monophosphate (cyclic AMP) mediate pharmacological inhibition of lysosomal discharge in leukocytes3,4 we reasoned that increased amounts of this nucleotide may occur in macrophages infected with living mycobacteria but not in those infected with dead ones. We report here experiments with M. microti showing that this is so and suggesting a bacterial origin for the addititional cyclic AMP.

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