New TB treatments hiding in plain sight.

Andrew J Olive,Christopher M Sassetti

doi:10.15252/emmm.201404815

Andrew J Olive, Christopher M Sassetti

Open Access

https://doi.org/10.15252/emmm.201404815

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Abstract

As tuberculosis (TB) toll is revised upward according to the WHO's last estimates, the lack of vaccine strategy and the lengthy antibiotic treatments that unfortunately promote the emergence of drug resistance are a major set back in the fight against this pathogen. In this issue of EMBO Molecular Medicine, Schiebler et al (Mtb) propose a novel and compelling new approach to target Mycobacterium tuberculosis (Mtb) by pharmacologically stimulating intracellular mycobacteria clearance through autophagy.

Highlights

As tuberculosis (TB) toll is revised upward according to the WHO’s last estimates, the lack of vaccine strategy and the lengthy antibiotic treatments that promote the emergence of drug resistance are a major set back in the fight against this pathogen
Recent studies have elucidated unexpected connections between metabolism and immune defense and suggest that new treatments for tuberculosis may lay hidden in our existing pharmacopeia
Factors limiting tuberculosis control include a huge burden of asymptomatic infection, the lack of a vaccine that protects from pulmonary disease, and lengthy antibiotic regimens that are being compromised by the continual emergence of drug-resistant strains (Casenghi et al, 2007; Nunes-Alves et al, 2014)

Summary

Introduction

As tuberculosis (TB) toll is revised upward according to the WHO’s last estimates, the lack of vaccine strategy and the lengthy antibiotic treatments that promote the emergence of drug resistance are a major set back in the fight against this pathogen. Recent studies have elucidated unexpected connections between metabolism and immune defense and suggest that new treatments for tuberculosis may lay hidden in our existing pharmacopeia. Mtb infection activates selective autophagy in phagocytes, known as xenophagy, which has been proposed to serve an antimicrobial function that restricts bacterial replication by targeting the intracellular bacterium to the inhospitable autophagosome.

Results

Conclusion