The Role of Epigenetics in Tuberculosis Infection

Abstract

Epigenetic mechanisms are pivotal in regulating gene expression during cellular response to extracellular stimuli. Bacterial infections have a profound effect on the host epigenome, which triggers susceptibility to diseases. Recent studies suggest that Mycobacterium tuberculosis (Mtb) can alter the host epigenome to modulate the transcriptional machinery and plays a major role in immunomodulation of the host immune response. However, the mechanism of epigenetic alterations during Mtb infection has not yet been fully understood. Thus, Mtb-induced epigenetic changes may affect the host cell by either activation or suppression of key immune genes involved in immune response or pathogen persistence. In this review, we discuss the principles of epigenetics, recent advances in Mtb-induced alterations in the host epigenetic landscape and their role in the host immune response.

Keywords: :

• epigenetics
• DNA methylation
• histone modifications
• immunity
• miRNA
• Mycobacterium tuberculosis
• tuberculosis

Supplementary data

To view the supplementary data that accompany this paper please visit the journal website at: http://www.tandfonline.com/doi/full/10.2217/epi.16.1

Acknowledgement

The authors thank I Hyder and S Chellappa for providing technical support and help preparing this manuscript.

Financial & competing interests disclosure

The authors greatly acknowledge Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER) Intramural Research grant (JIP/Res/Intra-PhD/01/2015-16/34) for financial support. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The authors greatly acknowledge Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER) Intramural Research grant (JIP/Res/Intra-PhD/01/2015-16/34) for financial support. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.