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We have recently shown that many mutants ofLegionella pneumophila exhibit similar defective phenotypes within both U937 human-derived macrophages and the protozoan hostAcanthamoeba (L.-Y. Gao, O. S. Harb, and Y. Abu Kwaik, Infect. Immun. 65:4738–4746, 1997). These observations have suggested that many of the mechanisms utilized byL. pneumophila to parasitize mammalian and protozoan cells are similar, but our data have not excluded the possibility that there are unique mechanisms utilized byL. pneumophila to survive and replicate within macrophages but not protozoa. To examine this possibility, we screened a bank of 5,280 miniTn10 ::kan transposon insertion mutants ofL. pneumophila for potential mutants that exhibited defective phenotypes of cytopathogenicity and intracellular replication within macrophage-like U937 cells but not withinAcanthamoeba polyphaga . We identified 32 mutants with various degrees of defects in cytopathogenicity, intracellular survival, and replication within human macrophages, and most of the mutants exhibited wild-type phenotypes within protozoa. Six of the mutants exhibited mild defects in protozoa. The defective loci were designatedmil (for macrophage-specific infectivity loci). Based on their intracellular growth defects within macrophages, themil mutants were grouped into five phenotypic groups. Groups I to III included the mutants that were severely defective in macrophages, while members of the other two groups exhibited a modestly defective phenotype within macrophages. The growth kinetics of many mutants belonging to groups I to III were also examined, and these were shown to have a similar defective phenotype in peripheral blood monocytes and a wild-type phenotype within another protozoan host,Hartmannella vermiformis . Transmission electron microscopy ofA. polyphaga infected by three of themil mutants belonging to groups I and II showed that they were similar to the parent strain in their capacity to recruit the rough endoplasmic reticulum (RER) around the phagosome. In contrast, infection of macrophages showed that the three mutants failed to recruit the RER around the phagosome during early stages of the infection. None of themil mutants was resistant to NaCl, and thedot oricm NaClr mutants are severely defective within mammalian and protozoan cells. Our data indicated that in addition to differences in mechanisms of uptake ofL. pneumophila by macrophages and protozoa, there were also genetic loci required forL. pneumophila to parasitize mammalian but not protozoan cells. We hypothesize thatL. pneumophila has evolved as a protozoan parasite in the environment but has acquired loci specific for intracellular replication within macrophages. Alternatively, ecological coevolution with protozoa has allowedL. pneumophila to possess multiple redundant mechanisms to parasitize protozoa and that some of these mechanisms do not function within macrophages.

infection and immunity

Identification of Macrophage-Specific Infectivity Loci ( <i>mil</i> ) of <i>Legionella pneumophila</i> That Are Not Required for Infectivity of Protozoa

Identification of Macrophage-Specific Infectivity Loci ( mil ) of Legionella pneumophila That Are Not Required for Infectivity of Protozoa