Cellular stress responses and immunological regulations during mycobacterium tuberculosis infection

Abstract

Tuberculosis (TB) is one of the most devastating infectious diseases caused by Mycobacterium tuberculosis (MTB). A high percentage of mortality and morbidity associated with TB has been reported globally with the highest number of cases reported in Asia. MTB is known to enter a state of dormancy and phenotypic drug resistance, when it is exposed to multiple stress conditions in the host microenvironment, and thereby it survives asymptomatically in latent phase in the host for decades and even for a lifetime. This raises the need for improved vaccine, drugs, and therapeutics, which could be achieved by a better understanding of the host-microbe interactions as well as immune responses during the infection. Recent studies have highlighted the importance of host cellular stress response pathways, such as unfolded protein response (UPR), oxidative stress response, integrated stress response (ISR), and autophagy during various infections. However, the role of these host stress response pathways during an MTB infection in the modulation of the immune response against the microbe is poorly understood. Therefore, through this chapter, we will highlight the cellular stress response pathways and various molecular mechanisms through which MTB influences the host innate as well as the adaptive immune response during infection, which might aid toward better design and development of therapeutics and vaccine candidates against TB.