title: Foamy macrophages and the progression of the human tuberculosis granuloma.
abstract: 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.
authors.affiliation: Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA. dgr8@cornell.edu
authors.forename: David G
authors.initials: DG
authors.lastname: Russell
authors.forename: Pere-Joan
authors.initials: PJ
authors.lastname: Cardona
authors.forename: Mi-Jeong
authors.initials: MJ
authors.lastname: Kim
authors.forename: Sophie
authors.initials: S
authors.lastname: Allain
authors.forename: Frédéric
authors.initials: F
authors.lastname: Altare
mesh_terms: 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
chemical_list: D008055:Lipids; D008077:Lipoproteins, LDL; D014409:Tumor Necrosis Factor-alpha; D007522:Isocitrate Lyase
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