Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-12-5
pubmed:abstractText
Tuberculosis is characterized by a tight interplay between Mycobacterium tuberculosis (M. tb) and host cells within granulomas. These cellular aggregates restrain M. tb spreading but do not kill all bacilli, which persist for years. A more detailed investigation of the interaction between M. tb and granuloma cells is needed to improve our understanding of this persistence and to explain the physiopathology of tuberculosis. In the present study, a recently developed in vitro human model of tuberculous granulomas has been used to analyse the modulation of granuloma cell differentiation by M. tb, in comparison to poorly virulent mycobacteria, which do not persist. It is reported that whilst all mycobacteria species induce granuloma formation, only M. tb triggers the differentiation of granuloma macrophages into very large multinucleated giant cells (MGCs) that are unable to mediate any bacterial uptake. This loss of function is not due to cell quiescence, as MGCs still display NADPH oxidase activity, but it correlates with decreased expression of phagocytosis receptors. This phenomenon is specific for the virulent species of M. tuberculosis complex, as poorly virulent species only induce the formation of small multinucleated cells (MCs) with conserved mycobacterial uptake ability, which never reach the MGC differentiation stage. The phenotype of MGCs thus strongly resembles mature dendritic cells with a loss of microbial uptake ability, despite conserved antigen presentation. In M. tb-induced granulomas, MGCs thus seem to be devoted to the destruction of bacilli that have been ingested in previous differentiation stages, ie in macrophages and MCs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-3417
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2006 Pathological Society of Great Britain and Ireland.
pubmed:issnType
Print
pubmed:volume
211
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
76-85
pubmed:meshHeading
pubmed-meshheading:17115379-Antigen-Presenting Cells, pubmed-meshheading:17115379-Axilla, pubmed-meshheading:17115379-BCG Vaccine, pubmed-meshheading:17115379-Flow Cytometry, pubmed-meshheading:17115379-Giant Cells, pubmed-meshheading:17115379-Giant Cells, Langhans, pubmed-meshheading:17115379-Granuloma, Giant Cell, pubmed-meshheading:17115379-Humans, pubmed-meshheading:17115379-Immunohistochemistry, pubmed-meshheading:17115379-Lymph Nodes, pubmed-meshheading:17115379-Microscopy, Confocal, pubmed-meshheading:17115379-Mycobacterium tuberculosis, pubmed-meshheading:17115379-NADP, pubmed-meshheading:17115379-Phagocytosis, pubmed-meshheading:17115379-Species Specificity, pubmed-meshheading:17115379-Staining and Labeling, pubmed-meshheading:17115379-Tuberculosis, pubmed-meshheading:17115379-Virulence
pubmed:year
2007
pubmed:articleTitle
Langhans giant cells from M. tuberculosis-induced human granulomas cannot mediate mycobacterial uptake.
pubmed:affiliation
Department Molecular Mechanisms of Mycobacterial Infections, IPBS, CNRS-UMR5089, Toulouse, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't