Autophagy in Mycobacterium tuberculosis infection: A passepartout to flush the intruder out?

Research output: Contribution to journalArticle

Abstract

Tuberculosis is a global health calamity. The causative agent, Mycobacterium tuberculosis (M. tuberculosis), has evolved elaborate survival mechanisms in humans, allowing it to remain in a clinically latent infection state, constantly engaging the immune system, with the possibility to progress to active disease. Autophagy is a cellular process responsible for the degradation of intracellular components, including invading pathogens, playing an important role in both innate and adaptive immunity.In this review, we describe the molecular mechanisms employed by M. tuberculosis to avoid autophagic degradation and exploit this process to its own advantage. Moreover, we discuss the multiple roles played by autophagy in the immune responses to M. tuberculosis, and its unforeseen contribution to the antibacterial activity of tuberculosis-specific drugs.

Original languageEnglish
Pages (from-to)335-343
Number of pages9
JournalCytokine and Growth Factor Reviews
Volume24
Issue number4
DOIs
Publication statusPublished - Aug 2013

Fingerprint

Mycobacterium Infections
Autophagy
Mycobacterium tuberculosis
Degradation
Immune system
Tuberculosis
Pathogens
Health
Adaptive Immunity
Innate Immunity
Immune System
Pharmaceutical Preparations
Survival
Infection

Keywords

  • Anti-tuberculosis drugs
  • Autophagy
  • Autophagy gene polymorphisms
  • Inflammatory cytokines
  • Mycobacterium tuberculosis

ASJC Scopus subject areas

  • Immunology
  • Endocrinology, Diabetes and Metabolism
  • Immunology and Allergy
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{61329cfa622743c8a490cf09f1ddc7a5,
title = "Autophagy in Mycobacterium tuberculosis infection: A passepartout to flush the intruder out?",
abstract = "Tuberculosis is a global health calamity. The causative agent, Mycobacterium tuberculosis (M. tuberculosis), has evolved elaborate survival mechanisms in humans, allowing it to remain in a clinically latent infection state, constantly engaging the immune system, with the possibility to progress to active disease. Autophagy is a cellular process responsible for the degradation of intracellular components, including invading pathogens, playing an important role in both innate and adaptive immunity.In this review, we describe the molecular mechanisms employed by M. tuberculosis to avoid autophagic degradation and exploit this process to its own advantage. Moreover, we discuss the multiple roles played by autophagy in the immune responses to M. tuberculosis, and its unforeseen contribution to the antibacterial activity of tuberculosis-specific drugs.",
keywords = "Anti-tuberculosis drugs, Autophagy, Autophagy gene polymorphisms, Inflammatory cytokines, Mycobacterium tuberculosis",
author = "Delia Goletti and Elisa Petruccioli and Alessandra Romagnoli and Mauro Piacentini and Fimia, {Gian Maria}",
year = "2013",
month = "8",
doi = "10.1016/j.cytogfr.2013.01.002",
language = "English",
volume = "24",
pages = "335--343",
journal = "Cytokine and Growth Factor Reviews",
issn = "1359-6101",
publisher = "Elsevier BV",
number = "4",

}

TY - JOUR

T1 - Autophagy in Mycobacterium tuberculosis infection

T2 - A passepartout to flush the intruder out?

AU - Goletti, Delia

AU - Petruccioli, Elisa

AU - Romagnoli, Alessandra

AU - Piacentini, Mauro

AU - Fimia, Gian Maria

PY - 2013/8

Y1 - 2013/8

N2 - Tuberculosis is a global health calamity. The causative agent, Mycobacterium tuberculosis (M. tuberculosis), has evolved elaborate survival mechanisms in humans, allowing it to remain in a clinically latent infection state, constantly engaging the immune system, with the possibility to progress to active disease. Autophagy is a cellular process responsible for the degradation of intracellular components, including invading pathogens, playing an important role in both innate and adaptive immunity.In this review, we describe the molecular mechanisms employed by M. tuberculosis to avoid autophagic degradation and exploit this process to its own advantage. Moreover, we discuss the multiple roles played by autophagy in the immune responses to M. tuberculosis, and its unforeseen contribution to the antibacterial activity of tuberculosis-specific drugs.

AB - Tuberculosis is a global health calamity. The causative agent, Mycobacterium tuberculosis (M. tuberculosis), has evolved elaborate survival mechanisms in humans, allowing it to remain in a clinically latent infection state, constantly engaging the immune system, with the possibility to progress to active disease. Autophagy is a cellular process responsible for the degradation of intracellular components, including invading pathogens, playing an important role in both innate and adaptive immunity.In this review, we describe the molecular mechanisms employed by M. tuberculosis to avoid autophagic degradation and exploit this process to its own advantage. Moreover, we discuss the multiple roles played by autophagy in the immune responses to M. tuberculosis, and its unforeseen contribution to the antibacterial activity of tuberculosis-specific drugs.

KW - Anti-tuberculosis drugs

KW - Autophagy

KW - Autophagy gene polymorphisms

KW - Inflammatory cytokines

KW - Mycobacterium tuberculosis

UR - http://www.scopus.com/inward/record.url?scp=84883797212&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84883797212&partnerID=8YFLogxK

U2 - 10.1016/j.cytogfr.2013.01.002

DO - 10.1016/j.cytogfr.2013.01.002

M3 - Article

C2 - 23395260

AN - SCOPUS:84883797212

VL - 24

SP - 335

EP - 343

JO - Cytokine and Growth Factor Reviews

JF - Cytokine and Growth Factor Reviews

SN - 1359-6101

IS - 4

ER -