Mycobacterium tuberculosis : Bacterial Fitness within the Host Macrophage

Mycobacterium tuberculosis has evolved to become the single greatest cause of death from an infectious agent. The pathogen spends most of its infection cycle in its human host within a phagocyte. The bacterium has evolved to block the normal maturation and acidification of its phagosome and resides...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Microbiology spectrum Jg. 7; H. 2
Hauptverfasser: Huang, Lu, Nazarova, Evgeniya V., Russell, David G.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States ASM Press 01.03.2019
Schlagworte:
Animals
Anti-Bacterial Agents - pharmacology
Cytokines - metabolism
Host-Pathogen Interactions
Humans
Macrophages
Macrophages - microbiology
Microbial Viability
Mycobacterium tuberculosis
Mycobacterium tuberculosis - drug effects
Mycobacterium tuberculosis - growth & development
Mycobacterium tuberculosis - metabolism
Mycobacterium tuberculosis - physiology
Pathogenesis
Phagocytes - microbiology
Phagosomes - microbiology
Tuberculosis
Tuberculosis - immunology
Tuberculosis - microbiology
Vacuoles - microbiology
ISSN:2165-0497, 2165-0497
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Mycobacterium tuberculosis has evolved to become the single greatest cause of death from an infectious agent. The pathogen spends most of its infection cycle in its human host within a phagocyte. The bacterium has evolved to block the normal maturation and acidification of its phagosome and resides in a vacuole contiguous with the early endosomal network. Cytokine-mediated activation of the host cell can overcome this blockage, and an array of antimicrobial responses can limit its survival. The survival of M. tuberculosis in its host cell is fueled predominantly by fatty acids and cholesterol. The ability of M. tuberculosis to degrade sterols is an unusual metabolic characteristic that was likely retained from a saprophytic ancestor. Recent results with fluorescent M. tuberculosis reporter strains demonstrate that bacterial survival differs with the host macrophage population. Tissue-resident alveolar macrophages, which are biased towards an alternatively activated, M2-like phenotype, are more permissive to bacterial growth than monocyte-derived, inflammatory, M1-like interstitial macrophages. The differential growth of the bacterium in these different phagocyte populations appears to be linked to host cell metabolism.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:2165-0497
2165-0497
DOI:10.1128/microbiolspec.BAI-0001-2019