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Updated: Dec 14, 2025
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Deacetylation Assays to Unravel the Interplay between Sirtuins SIRT2 and Specific Protein-substrates
Published on: February 27, 2016
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Host sirtuin 2 as an immunotherapeutic target against tuberculosis
Ashima Bhaskar1, Santosh Kumar2, Mehak Zahoor Khan1
1Signal Transduction Laboratory 1, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, India.
Elife
|July 23, 2020
Summary
Mycobacterium tuberculosis hijacks host immunity by upregulating Sirtuin 2 (SIRT2), an epigenetic regulator. Inhibiting SIRT2 restricts bacterial growth and enhances tuberculosis drug efficacy.
Area of Science:
- Immunology
- Epigenetics
- Microbiology
Background:
- Mycobacterium tuberculosis (Mtb) utilizes host defense mechanisms for survival.
- Epigenetic modifications play a crucial role in host-pathogen interactions.
Purpose of the Study:
- To investigate the role of NAD+ dependent histone deacetylase Sirtuin 2 (SIRT2) in Mtb infection.
- To explore SIRT2 as a therapeutic target for tuberculosis.
Main Methods:
- Studied SIRT2 upregulation and nuclear translocation upon Mtb infection.
- Investigated SIRT2's deacetylation of histone H3K18 and NFκB-p65.
- Evaluated the efficacy of pharmacological SIRT2 inhibition in a murine model.
Main Results:
- Mtb infection upregulates SIRT2, which modulates host transcriptome and macrophage activation.
- SIRT2 deacetylates NFκB-p65 in T cells, affecting T helper cell differentiation.
- SIRT2 inhibition reduced Mtb growth, enhanced Isoniazid efficacy, decreased pathology, and boosted immune responses in mice.
Conclusions:
- SIRT2 links Mtb infection, epigenetics, and host immune response.
- Targeting SIRT2 offers a potential therapeutic strategy against tuberculosis, including drug-resistant strains.
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