Phagosomal membranes of Mycobacterium bovis BCG-immune alveolar macrophages are resistant to disruption by Mycobacterium tuberculosis H37Rv

Leake, Eva S.; Myrvik, Quentin N.; Wright, Mary Jo

doi:10.1128/iai.45.2.443-446.1984

Cited by 42 publications

(19 citation statements)

References 4 publications

(1 reference statement)

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“…On the other hand, one report states that virulent M. tuberculosis H37Rv bacilli can escape from the phagosome into the cytosol of normal rabbit alveolar macrophages whereas attenuated H37Ra bacilli cannot (26). Interestingly, a related study showed that the attenuated vaccine strain M. bovis BCG was also capable of escaping from the phagosomal membrane in normal rabbit alveolar macrophages although only a maximum of 25% of the ingested bacilli were found free in the cytoplasm (19). This study is in contrast to our findings, in which we were unable to show any cytolytic activity by this strain.…”

Section: The Plasmids Puc19 and Pbluescript Ii's-(stratagene)contrasting

confidence: 99%

Expression of contact-dependent cytolytic activity by Mycobacterium tuberculosis and isolation of the genomic locus that encodes the activity

et al. 1993

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We investigated the presence of cytolytic activity in the virulent H37Rv and attenuated H37Ra strains of Mycobacterium tuberculosis and in the vaccine strain Mycobacterium bovis BCG. The virulent strain H37Rv expressed >3-fold more contact-dependent cytolytic activity than the attenuated strain H37Ra, and the vaccine strain M. bovis BCG did not produce cytolytic activity. We also isolated an-3.2-kbp fragment of the M. tuberculosis H37Rv genome that was capable of inducing this contact-dependent hemolytic activity in a nonhemolytic strain of Escherichia coli.

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Section: The Plasmids Puc19 and Pbluescript Ii's-(stratagene)contrasting

confidence: 99%

Expression of contact-dependent cytolytic activity by Mycobacterium tuberculosis and isolation of the genomic locus that encodes the activity

et al. 1993

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“…The first reports of mycobacterial cytosolic localization are from 1984 (Leake et al ., 1984; Myrvik et al ., 1984); however, we are only now beginning to understand why this subcellular event is so often overlooked. Translocation, also often termed ‘escape’ is, however, well established as a virulence mechanism in several bacteria from other genera, including Shigella flexneri , Listeria monocytogenes , Burkholderia pseudomallei , Neisseria meningitidis , Rickettsia prowazekii and Francisella tularensis (Ray et al ., 2009).…”

Section: Resultsmentioning

confidence: 99%

ESX‐1‐mediated translocation to the cytosol controls virulence of mycobacteria

Houben

Demangel

Ingen

et al. 2012

Cellular Microbiology

376

383

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SummaryMycobacterium species, including Mycobacterium tuberculosis and Mycobacterium leprae, are among the most potent human bacterial pathogens. The discovery of cytosolic mycobacteria challenged the paradigm that these pathogens exclusively localize within the phagosome of host cells. As yet the biological relevance of mycobacterial translocation to the cytosol remained unclear. In this current study we used electron microscopy techniques to establish a clear link between translocation and mycobacterial virulence. Pathogenic, patientderived mycobacteria species were found to translocate to the cytosol, while non-pathogenic species did not. We were further able to link cytosolic translocation with pathogenicity by introducing the ESX-1 (type VII) secretion system into the nonvirulent, exclusively phagolysosomal Mycobacterium bovis BCG. Furthermore, we show that translocation is dependent on the C-terminus of the early-secreted antigen ESAT-6. The C-terminal truncation of ESAT-6 was shown to result in attenuation in mice, again linking translocation to virulence. Together, these data demonstrate the molecular mechanism facilitating translocation of mycobacteria. The ability to translocate from the phagolysosome to the cytosol is with this study proven to be biologically significant as it determines mycobacterial virulence.

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“…There have been reports over time providing evidence that M.tb can translocate into the cytosol of macrophages under defined conditions (Leake et al ., 1984; Myrvik et al ., 1984; McDonough et al ., 1993; van der Wel et al ., 2007) and also that mycobacterial phagosomes are porous (Teitelbaum et al ., 1999). Nonetheless, the weight of the evidence to date is that mycobacteria replicate in phagosomes in human and mouse macrophages.…”

Section: Discussionmentioning

confidence: 99%

NOD2 controls the nature of the inflammatory response and subsequent fate of Mycobacterium tuberculosis and M. bovis BCG in human macrophages

Brooks

Rajaram

Azad

et al. 2010

Cellular Microbiology

123

105

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Summary Mycobacterium tuberculosis (M.tb), which causes tuberculosis, is a host-adapted intracellular pathogen of macrophages. Intracellular pattern recognition receptors in macrophages such as nucleotide-binding oligomerization domain (NOD) proteins regulate pro-inflammatory cytokine production. NOD2-mediated signalling pathways in response to M.tb have been studied primarily in mouse models and cell lines but not in primary human macrophages. Thus we sought to determine the role of NOD2 in regulating cytokine production and growth of virulent M.tb and attenuated Mycobacterium bovis BCG (BCG) in human macrophages. We examined NOD2 expression during monocyte differentiation and observed a marked increase in NOD2 transcript and protein following 2–3 days in culture. Pre-treatment of human monocyte-derived and alveolar macrophages with the NOD2 ligand muramyl dipeptide enhanced production of TNF-α and IL-1β in response to M.tb and BCG in a RIP2-dependent fashion. The NOD2-mediated cytokine response was significantly reduced following knock-down of NOD2 expression by using small interfering RNA (siRNA) in human macrophages. Finally, NOD2 controlled the growth of both M.tb and BCG in human macrophages, whereas controlling only BCG growth in murine macrophages. Together, our results provide evidence that NOD2 is an important intracellular receptor in regulating the host response to M.tb and BCG infection in human macrophages.

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Phagosomal membranes of Mycobacterium bovis BCG-immune alveolar macrophages are resistant to disruption by Mycobacterium tuberculosis H37Rv

Cited by 42 publications

References 4 publications

Expression of contact-dependent cytolytic activity by Mycobacterium tuberculosis and isolation of the genomic locus that encodes the activity

Expression of contact-dependent cytolytic activity by Mycobacterium tuberculosis and isolation of the genomic locus that encodes the activity

ESX‐1‐mediated translocation to the cytosol controls virulence of mycobacteria

NOD2 controls the nature of the inflammatory response and subsequent fate of Mycobacterium tuberculosis and M. bovis BCG in human macrophages

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