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Am J Physiol Lung Cell Mol Physiol. 2017 Aug 1;313(2):L218-L229. doi: 10.1152/ajplung.00162.2017. Epub 2017 May 11.

Role of apoptosis and autophagy in tuberculosis.

Author information

1
Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and.
2
Medical College of Georgia, Augusta University, Augusta, Georgia.
3
Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and saurabhaggarwal@uabmc.edu.

Abstract

Tuberculosis (TB) is one of the oldest known human diseases and is transmitted by the bacteria Mycobacterium tuberculosis (Mtb). TB has a rich history with evidence of TB infections dating back to 5,800 bc TB is unique in its ability to remain latent in an individual for decades, with the possibility of later reactivation, causing widespread systemic symptoms. Currently, it is estimated that more than one-third of the world's population (~2 billion people) are infected with Mtb. Prolonged periods of therapy and complexity of treatment regimens, especially in active infection, have led to poor compliance in patients being treated for TB. Therefore, it is vitally important to have a thorough knowledge of the pathophysiology of Mtb to understand the disease progression, as well as to develop novel diagnostic tests and treatments. Alveolar macrophages represent both the primary host cell and the first line of defense against the Mtb infection. Apoptosis and autophagy of macrophages play a vital role in the pathogenesis and also in the host defense against Mtb. This review will outline the role of these two cellular processes in defense against Mtb with particular emphasis on innate immunity and explore developing therapies aimed at altering host responses to the disease.

KEYWORDS:

apoptosis; autophagy; endoplasmic reticulum stress; tuberculosis

PMID:
28495854
PMCID:
PMC5582934
DOI:
10.1152/ajplung.00162.2017
[Indexed for MEDLINE]
Free PMC Article

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