Foamy macrophages and the progression of the human tuberculosis granuloma.
The progression of tuberculosis from a latent, subclinical infection to active disease that culminates in the transmission of infectious bacilli is determined locally at the level of the granuloma. This progression takes place even in the face of a robust immune response that, although it contains infection, is unable to eliminate the bacterium. The factors or environmental conditions that influence this progression remain to be determined. Recent advances have indicated that pathogen-induced dysregulation of host lipid synthesis and sequestration serves a critical role in this transition. The foamy macrophage seems to be a key participant in both sustaining persistent bacteria and contributing to the tissue pathology that leads to cavitation and the release of infectious bacilli.
Russell
David G
DG
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA. dgr8@cornell.edu
Cardona
Pere-Joan
PJ
Kim
Mi-Jeong
MJ
Allain
Sophie
S
Altare
Frédéric
F
D000818:Animals; D018450:Disease Progression; D005487:Foam Cells / Q000502:physiology*; D006099:Granuloma / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D006801:Humans; D007522:Isocitrate Lyase / Q000502:physiology; D008055:Lipids / Q000096:biosynthesis; D008077:Lipoproteins, LDL / Q000378:metabolism; D010588:Phagosomes / Q000502:physiology; D014376:Tuberculosis / Q000276:immunology* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D008055:Lipids; D008077:Lipoproteins, LDL; D014409:Tumor Necrosis Factor-alpha; D007522:Isocitrate Lyase
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