A parallel intraphagosomal survival strategy shared by Mycobacterium tuberculosis and Salmonella enterica

Mycobacterium tuberculosis and Salmonella enterica cause very different diseases and are only distantly related. However, growth within macrophages is crucial for virulence in both of these intracellular pathogens. Here, we demonstrate that in spite of the phylogenetic distance, M. tuberculosis and...

Full description

Saved in:
Bibliographic Details
Published in:Molecular microbiology 2000-03, Vol.35 (6), p.1375-1382
Main Authors: Buchmeier, Nancy, Blanc‐Potard, Anne, Ehrt, Sabine, Piddington, Debra, Riley, Lee, Groisman, Eduardo A.
Format: Article
Language:English
Subjects:
Animals
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cation Transport Proteins
Cell Division - drug effects
Cell Division - genetics
Female
Humans
Hydrogen-Ion Concentration
Life Sciences
Macrophages - microbiology
Magnesium - pharmacology
mgtC gene
Mice
Mice, Inbred BALB C
Mutation
Mycobacterium tuberculosis
Mycobacterium tuberculosis - pathogenicity
Mycobacterium tuberculosis - physiology
phagosomes
Phagosomes - microbiology
Salmonella enterica
Salmonella enterica - pathogenicity
Salmonella enterica - physiology
Species Specificity
Virulence
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Mycobacterium tuberculosis and Salmonella enterica cause very different diseases and are only distantly related. However, growth within macrophages is crucial for virulence in both of these intracellular pathogens. Here, we demonstrate that in spite of the phylogenetic distance, M. tuberculosis and Salmonella employ a parallel survival strategy for growth within macrophage phagosomes. Previous studies established that the Salmonella mgtC gene is required for growth within macrophages and for virulence in vivo. M. tuberculosis contains an open reading frame exhibiting 38% amino acid identity with the Salmonella MgtC protein. Upon inactivation of mgtC, the resulting M. tuberculosis mutant was attenuated for virulence in cultured human macrophages and impaired for growth in the lungs and spleens of mice. Replication of the mgtC mutant was inhibited in vitro by a combination of low magnesium and mildly acidic pH suggesting that the M. tuberculosis‐containing phagosome has these characteristics. The similar phenotypes displayed by the mgtC mutants of M. tuberculosis and Salmonella suggest that the ability to acquire magnesium is essential for virulence in intracellular pathogens that proliferate within macrophage phagosomes.
ISSN:0950-382X
1365-2958
DOI:10.1046/j.1365-2958.2000.01797.x