Open AccessInactivation of the Mycobacterium tuberculosis Nramp orthologue ( mntH ) does not affect virulence in a mouse model of tuberculosis
Author(s) -
Domenech P,
Pym A.S.,
Cellier M,
Barry C.E.,
Cole S.T.
Publication year - 2002
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2002.tb11032.x
Subject(s) - virulence , mycobacterium tuberculosis , tuberculosis , macrophage , mutant , biology , intracellular , microbiology and biotechnology , pathogen , gene , genetics , medicine , in vitro , pathology
Mycobacterium tuberculosis is an intracellular pathogen which can survive and multiply within the phagosomal compartment of the macrophage, and in doing so has to withstand the various macrophage defense mechanisms, which include limitation of iron and other metals. Analysis of the complete genome sequence of M. tuberculosis revealed an extensive array of cation transporters, including mntH , an orthologue of the eukaryotic Nramp (natural resistance‐associated macrophage protein) gene, that encodes a proton‐dependent divalent metal transporter. To assess the effect of this transporter on intracellular survival and pathogenesis, an mntH knock‐out mutant of M. tuberculosis H37Rv was created and assayed in bone marrow‐derived macrophages and in a murine model of tuberculosis. In neither of these systems was any loss of fitness associated with inactivation of mntH , demonstrating that Nramp orthologues are not important determinants of mycobacterial virulence.