Epigenetics in Tuberculosis: Immunomodulation of Host Immune Response

Abstract

Tuberculosis is a stern, difficult to treat chronic infection caused by acid-fast bacilli that tend to take a long time to be eradicated from the host’s environment. It requires the action of both innate and adaptive immune systems by the host. There are various pattern recognition receptors present on immune cells, which recognize foreign pathogens or its product and trigger the immune response. The epigenetic modification plays a crucial role in triggering the susceptibility of the host towards the pathogen and activating the host’s immune system against the invading pathogen. It alters the gene expression modifying the genetic material of the host’s cell. Epigenetic modification such as histone acetylation, alteration in non-coding RNA, DNA methylation and alteration in miRNA has been studied for their influence on the pathophysiology of tuberculosis to control the spread of infection. Despite several studies being conducted, many gaps still exist. Herein, we discuss the immunopathophysiological mechanism of tuberculosis, the essentials of epigenetics and the recent encroachment of epigenetics in the field of tuberculosis and its influence on the outcome and pathophysiology of the infection.

A host-directed oxadiazole compound potentiates antituberculosis treatment via zinc poisoning in human macrophages and in a mouse model of infection

“…We and others have previously shown that numerous epigenetic modifications occur in myeloid cells upon MTB infection [ 11 – 13 ]. These changes are either part of the initiation of the host response or an immune escape mechanism from MTB.…”

“…These changes are either part of the initiation of the host response or an immune escape mechanism from MTB. MTB indeed manipulates epigenetic host-signaling pathways to subvert host immunity [ 11 ]. Reprogramming the host immune system by a compound targeting the host epigenome may thus lead to a better control of the bacterial infection [ 14 ].…”

Exploring TSPAN4 promoter methylation as a diagnostic biomarker for tuberculosis

“…In summary, DNA methylation serves as a biomarker for tuberculosis diagnosis, with whole blood DNA methylation status detection proving effective. Additionally, methylation acts as a regulatory marker for immunopathology (Chen et al, 2020;Khadela et al, 2022), and it holds potential as a therapeutic and Frontiers in Genetics frontiersin.org prognostic marker in various diseases (Gampenrieder et al, 2018;Guo et al, 2019;Chen et al, 2020;Liang et al, 2022), with the possibility of future application in tuberculosis. Optimization and application of methylation detection methods are beneficial for diagnosing tuberculosis in high-incidence and economically challenged regions.…”

Immune-endocrine network in diabetes-tuberculosis nexus: does latent tuberculosis infection confer protection against meta-inflammation and insulin resistance?

“…Similarly LTBI, has been shown to have strong immunomodulatory effect, which in turn, can confer protection against IR ( 107 ). However, with urbanization (abundance of carbohydrate rich food, lack of physical activity and chronic stress) increased insulin demand leads to insulin deficiency, which along with IR precipitates into diabetes, even in LTBI subjects ( 108 ).…”