PAGES: DOI: 10.1590/0074-02760170281 Full paper
Mycobacterium tuberculosis promotes genomic instability in macrophages

Jorge Castro-Garza1, Miriam Lorena Luévano-Martínez1,2, Licet Villarreal-Treviño2, Jaime Gosálvez3, José Luis Fernández4, Martha Imelda Dávila-Rodríguez1, Catalina García-Vielma1, Silvia González-Hernández1, Elva Irene Cortés-Gutiérrez1,+

1Centro de Investigación Biomédica del Noreste, Instituto Mexicano del Seguro Social, Monterrey, NL, México
2Universidad Autónoma de Nuevo León, Facultad de Ciencias Biológicas, Monterrey, NL, México
3Universidad Autónoma de Madrid, Unit of Genetics, Department of Biology, Madrid, Spain
4Genetics Unit, Complejo Hospitalario Universitario A Coruña, La Coruña, Spain


BACKGROUND Mycobacterium tuberculosis is an intracellular pathogen, which may either block cellular defensive mechanisms and survive inside the host cell or induce cell death. Several studies are still exploring the mechanisms involved in these processes.

OBJECTIVES To evaluate the genomic instability of M. tuberculosis-infected macrophages and compare it with that of uninfected macrophages.

METHODS We analysed the possible variations in the genomic instability of Mycobacterium-infected macrophages using the DNA breakage detection fluorescence in situ hybridisation (DBD-FISH) technique with a whole human genome DNA probe.

FINDINGS Quantitative image analyses showed a significant increase in DNA damage in infected macrophages as compared with uninfected cells. DNA breaks were localised in nuclear membrane blebs, as confirmed with DNA fragmentation assay. Furthermore, a significant increase in micronuclei and nuclear abnormalities were observed in infected macrophages versus uninfected cells.

MAIN CONCLUSIONS Genomic instability occurs during mycobacterial infection and these data may be seminal for future research on host cell DNA damage in M. tuberculosis infection.

+ Corresponding author: This e-mail address is being protected from spambots. You need JavaScript enabled to view it.
Received 13 July 2017
Accepted 31 Oct 2017


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