Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Jun;5(3):10.1128/microbiolspec.tbtb2-0028-2016.
doi: 10.1128/microbiolspec.TBTB2-0028-2016.

Killing Mycobacterium tuberculosis In Vitro: What Model Systems Can Teach Us

Affiliations
Review

Killing Mycobacterium tuberculosis In Vitro: What Model Systems Can Teach Us

Tracy L Keiser et al. Microbiol Spectr. 2017 Jun.

Abstract

Tuberculosis is one of the most successful human diseases in our history due in large part to the multitude of virulence factors exhibited by the causative agent, Mycobacterium tuberculosis. Understanding the pathogenic nuances of this organism in the context of its human host is an ongoing topic of study facilitated by isolating cells from model organisms such as mice and non-human primates. However, M. tuberculosis is an obligate intracellular human pathogen, and disease progression and outcome in these model systems can differ from that of human disease. Current in vitro models of infection include primary macrophages and macrophage-like immortalized cell lines as well as the induced pluripotent stem cell-derived cell types. This article will discuss these in vitro model systems in general, what we have learned so far about utilizing them to answer questions about pathogenesis, the potential role of other cell types in innate control of M. tuberculosis infection, and the development of new coculture systems with multiple cell types. As we continue to expand current in vitro systems and institute new ones, the knowledge gained will improve our understanding of not only tuberculosis but all infectious diseases.

PubMed Disclaimer

References

    1. Anastasiou E, Mitchell PD. 2013. Palaeopathology and genes: investigating the genetics of infectious diseases in excavated human skeletal remains and mummies from past populations. Gene 528:33–40 10.1016/j.gene.2013.06.017. - DOI - PubMed
    1. Comas I, Coscolla M, Luo T, Borrell S, Holt KE, Kato-Maeda M, Parkhill J, Malla B, Berg S, Thwaites G, Yeboah-Manu D, Bothamley G, Mei J, Wei L, Bentley S, Harris SR, Niemann S, Diel R, Aseffa A, Gao Q, Young D, Gagneux S. 2013. Out-of-Africa migration and Neolithic coexpansion of Mycobacterium tuberculosis with modern humans. Nat Genet 45:1176–1182 10.1038/ng.2744. - DOI - PMC - PubMed
    1. Hmama Z, Peña-Díaz S, Joseph S, Av-Gay Y. 2015. Immunoevasion and immunosuppression of the macrophage by Mycobacterium tuberculosis. Immunol Rev 264:220–232 10.1111/imr.12268. [PubMed] - DOI - PubMed
    1. Murray PJ, Wynn TA. 2011. Protective and pathogenic functions of macrophage subsets. Nat Rev Immunol 11:723–737 10.1038/nri3073. [PubMed] - DOI - PMC - PubMed
    1. Khan N, Vidyarthi A, Javed S, Agrewala JN. 2016. Innate immunity holding the flanks until reinforced by adaptive immunity against Mycobacterium tuberculosis infection. Front Microbiol 7:328 10.3389/fmicb.2016.00328. - DOI - PMC - PubMed