rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2008-6-20
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pubmed:abstractText |
Mycobacterium tuberculosis possesses a diversity of potential virulence factors including complex branched lipids such as the phenolic glycolipid PGL-tb. PGL-tb expression by the clinical M. tuberculosis isolate HN878 has been associated with a less efficient Th1 response and increased virulence in mice and rabbits. It has been suggested that the W-Beijing family is the only group of M. tuberculosis strains with an intact pks1-15 gene, required for the synthesis of PGL-tb and capable of producing PGL-tb. We have found that some strains with an intact pks1-15 do not produce PGL-tb while others may produce a variant of PGL-tb. We examined the early host cytokine response to infection with these strains in vitro to better understand the effect of PGL-tb synthesis on immune responses. In addition, we generated a PGL-tb-producing H37Rv in order to determine the effect of PGL-tb production on the host immune response during infection by a strain normally devoid of PGL-tb synthesis. We observed that PGL-tb production by clinical M. tuberculosis isolates affected cytokine production differently depending on the background of the strain. Importantly, while ectopic PGL-tb production by H37Rv suppressed the induction of several pro- and anti-inflammatory cytokines in vitro in human monocytes, it did not lead to increased virulence in infected mice and rabbits. Collectively, our data indicate that, while PGL-tb may play a role in the immunogenicity and/or virulence of M. tuberculosis, it probably acts in concert with other bacterial factors which seem to be dependent on the background of the strain.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18443098-10352293,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/18443098-9634230
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Jul
|
pubmed:issn |
1098-5522
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pubmed:author |
pubmed-author:GuilhotChristopheC,
pubmed-author:HuetGaelleG,
pubmed-author:KanaBaveshB,
pubmed-author:KaplanGillaG,
pubmed-author:KooMi-SunMS,
pubmed-author:KreiswirthBarry NBN,
pubmed-author:KurepinaNataliaN,
pubmed-author:MancaClaudiaC,
pubmed-author:MarrasSalvatore A ESA,
pubmed-author:MathemaBarunB,
pubmed-author:SinsimerDanielD,
pubmed-author:TsenovaLianaL
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pubmed:issnType |
Electronic
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pubmed:volume |
76
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3027-36
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:18443098-Animals,
pubmed-meshheading:18443098-Antigens, Bacterial,
pubmed-meshheading:18443098-Cells, Cultured,
pubmed-meshheading:18443098-Cytokines,
pubmed-meshheading:18443098-Glycolipids,
pubmed-meshheading:18443098-Humans,
pubmed-meshheading:18443098-Leukocytes, Mononuclear,
pubmed-meshheading:18443098-Mice,
pubmed-meshheading:18443098-Monocytes,
pubmed-meshheading:18443098-Mycobacterium tuberculosis,
pubmed-meshheading:18443098-Rabbits,
pubmed-meshheading:18443098-Species Specificity,
pubmed-meshheading:18443098-Tuberculosis, Pulmonary,
pubmed-meshheading:18443098-Virulence
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pubmed:year |
2008
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pubmed:articleTitle |
The phenolic glycolipid of Mycobacterium tuberculosis differentially modulates the early host cytokine response but does not in itself confer hypervirulence.
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pubmed:affiliation |
Laboratory of Mycobacterial Immunity and Pathogenesis, Public Health Research Institute Center, University of Medicine and Dentistry of New Jersey, 225 Warren St., Newark, NJ 07103, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|