Macrophages and tuberculosis

Clíona Ní Cheallaigh, Celia Peral de Castro, Michelle M. Coleman, Jayne C. Hope, James Harris

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Researchpeer-review

Abstract

Mycobacterium tuberculosis and M. bovis, the causative agents of human and bovine tuberculosis (TB), respectively, have evolved efficient and potent mechanisms to enable their survival within macrophages. In particular, by preventing the fusion of phagosomes with lysosomes, mycobacteria are able to regulate their environment, free from acidification and lysosomal hydrolases. The bacilli are also able to hijack the cytokine responses of the macrophage and dampen the host's protective immune responses, promoting the secretion of anti-inflammatory cytokines and dampening TNF-α-dependent host protective responses. In turn, macrophages have developed ways to overcome these restraints imposed by the bacteria. Induction of autophagy by environmental stresses, such as nutrient or growth factor deprivation, Th1 cytokines (TNF-αand IFN-γ ) and pathogen-associated molecular patterns (PAMPs) leads to the intracellular elimination of mycobacteria by macrophages. In addition, autophagy is potentially involved in antigen processing and presentation and regulates the secretion of some cytokines. Finally, some receptors and their signalling molecules, including Tolllike Receptor (TLR)2 and TLR4, the scavenger receptor MARCO and MyD88 have been shown to be important in host-protective responses. This review summarises the current literature regarding the close and pivotal interactions between macrophages and mycobacteria that, in turn, determine the outcome of infection with these important intracellular pathogens.

Original languageEnglish
Title of host publicationHandbook of Macrophages: Life Cycle, Functions and Diseases
EditorsRikiya Takahashi, Hibiki Kai
Place of PublicationUnited Kingdom
PublisherNova Science Publishers
Pages1-41
Number of pages41
ISBN (Print)9781620811627
Publication statusPublished - Mar 2012
Externally publishedYes

Keywords

  • Apoptosis
  • Autophagy
  • Inflammation
  • Phagosome maturation
  • Th1
  • Th2

Cite this

Cheallaigh, C. N., de Castro, C. P., Coleman, M. M., Hope, J. C., & Harris, J. (2012). Macrophages and tuberculosis. In R. Takahashi, & H. Kai (Eds.), Handbook of Macrophages: Life Cycle, Functions and Diseases (pp. 1-41). United Kingdom: Nova Science Publishers.
Cheallaigh, Clíona Ní ; de Castro, Celia Peral ; Coleman, Michelle M. ; Hope, Jayne C. ; Harris, James. / Macrophages and tuberculosis. Handbook of Macrophages: Life Cycle, Functions and Diseases. editor / Rikiya Takahashi ; Hibiki Kai. United Kingdom : Nova Science Publishers, 2012. pp. 1-41
@inbook{6f54e63098844ba8ad64733cd2a2a881,
title = "Macrophages and tuberculosis",
abstract = "Mycobacterium tuberculosis and M. bovis, the causative agents of human and bovine tuberculosis (TB), respectively, have evolved efficient and potent mechanisms to enable their survival within macrophages. In particular, by preventing the fusion of phagosomes with lysosomes, mycobacteria are able to regulate their environment, free from acidification and lysosomal hydrolases. The bacilli are also able to hijack the cytokine responses of the macrophage and dampen the host's protective immune responses, promoting the secretion of anti-inflammatory cytokines and dampening TNF-α-dependent host protective responses. In turn, macrophages have developed ways to overcome these restraints imposed by the bacteria. Induction of autophagy by environmental stresses, such as nutrient or growth factor deprivation, Th1 cytokines (TNF-αand IFN-γ ) and pathogen-associated molecular patterns (PAMPs) leads to the intracellular elimination of mycobacteria by macrophages. In addition, autophagy is potentially involved in antigen processing and presentation and regulates the secretion of some cytokines. Finally, some receptors and their signalling molecules, including Tolllike Receptor (TLR)2 and TLR4, the scavenger receptor MARCO and MyD88 have been shown to be important in host-protective responses. This review summarises the current literature regarding the close and pivotal interactions between macrophages and mycobacteria that, in turn, determine the outcome of infection with these important intracellular pathogens.",
keywords = "Apoptosis, Autophagy, Inflammation, Phagosome maturation, Th1, Th2",
author = "Cheallaigh, {Cl{\'i}ona N{\'i}} and {de Castro}, {Celia Peral} and Coleman, {Michelle M.} and Hope, {Jayne C.} and James Harris",
year = "2012",
month = "3",
language = "English",
isbn = "9781620811627",
pages = "1--41",
editor = "Rikiya Takahashi and Hibiki Kai",
booktitle = "Handbook of Macrophages: Life Cycle, Functions and Diseases",
publisher = "Nova Science Publishers",
address = "United States of America",

}

Cheallaigh, CN, de Castro, CP, Coleman, MM, Hope, JC & Harris, J 2012, Macrophages and tuberculosis. in R Takahashi & H Kai (eds), Handbook of Macrophages: Life Cycle, Functions and Diseases. Nova Science Publishers, United Kingdom, pp. 1-41.

Macrophages and tuberculosis. / Cheallaigh, Clíona Ní; de Castro, Celia Peral; Coleman, Michelle M.; Hope, Jayne C.; Harris, James.

Handbook of Macrophages: Life Cycle, Functions and Diseases. ed. / Rikiya Takahashi; Hibiki Kai. United Kingdom : Nova Science Publishers, 2012. p. 1-41.

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Researchpeer-review

TY - CHAP

T1 - Macrophages and tuberculosis

AU - Cheallaigh, Clíona Ní

AU - de Castro, Celia Peral

AU - Coleman, Michelle M.

AU - Hope, Jayne C.

AU - Harris, James

PY - 2012/3

Y1 - 2012/3

N2 - Mycobacterium tuberculosis and M. bovis, the causative agents of human and bovine tuberculosis (TB), respectively, have evolved efficient and potent mechanisms to enable their survival within macrophages. In particular, by preventing the fusion of phagosomes with lysosomes, mycobacteria are able to regulate their environment, free from acidification and lysosomal hydrolases. The bacilli are also able to hijack the cytokine responses of the macrophage and dampen the host's protective immune responses, promoting the secretion of anti-inflammatory cytokines and dampening TNF-α-dependent host protective responses. In turn, macrophages have developed ways to overcome these restraints imposed by the bacteria. Induction of autophagy by environmental stresses, such as nutrient or growth factor deprivation, Th1 cytokines (TNF-αand IFN-γ ) and pathogen-associated molecular patterns (PAMPs) leads to the intracellular elimination of mycobacteria by macrophages. In addition, autophagy is potentially involved in antigen processing and presentation and regulates the secretion of some cytokines. Finally, some receptors and their signalling molecules, including Tolllike Receptor (TLR)2 and TLR4, the scavenger receptor MARCO and MyD88 have been shown to be important in host-protective responses. This review summarises the current literature regarding the close and pivotal interactions between macrophages and mycobacteria that, in turn, determine the outcome of infection with these important intracellular pathogens.

AB - Mycobacterium tuberculosis and M. bovis, the causative agents of human and bovine tuberculosis (TB), respectively, have evolved efficient and potent mechanisms to enable their survival within macrophages. In particular, by preventing the fusion of phagosomes with lysosomes, mycobacteria are able to regulate their environment, free from acidification and lysosomal hydrolases. The bacilli are also able to hijack the cytokine responses of the macrophage and dampen the host's protective immune responses, promoting the secretion of anti-inflammatory cytokines and dampening TNF-α-dependent host protective responses. In turn, macrophages have developed ways to overcome these restraints imposed by the bacteria. Induction of autophagy by environmental stresses, such as nutrient or growth factor deprivation, Th1 cytokines (TNF-αand IFN-γ ) and pathogen-associated molecular patterns (PAMPs) leads to the intracellular elimination of mycobacteria by macrophages. In addition, autophagy is potentially involved in antigen processing and presentation and regulates the secretion of some cytokines. Finally, some receptors and their signalling molecules, including Tolllike Receptor (TLR)2 and TLR4, the scavenger receptor MARCO and MyD88 have been shown to be important in host-protective responses. This review summarises the current literature regarding the close and pivotal interactions between macrophages and mycobacteria that, in turn, determine the outcome of infection with these important intracellular pathogens.

KW - Apoptosis

KW - Autophagy

KW - Inflammation

KW - Phagosome maturation

KW - Th1

KW - Th2

UR - http://www.scopus.com/inward/record.url?scp=84881547633&partnerID=8YFLogxK

M3 - Chapter (Book)

SN - 9781620811627

SP - 1

EP - 41

BT - Handbook of Macrophages: Life Cycle, Functions and Diseases

A2 - Takahashi, Rikiya

A2 - Kai, Hibiki

PB - Nova Science Publishers

CY - United Kingdom

ER -

Cheallaigh CN, de Castro CP, Coleman MM, Hope JC, Harris J. Macrophages and tuberculosis. In Takahashi R, Kai H, editors, Handbook of Macrophages: Life Cycle, Functions and Diseases. United Kingdom: Nova Science Publishers. 2012. p. 1-41