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rdf:type |
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lifeskim:mentions |
umls-concept:C0021753,
umls-concept:C0026926,
umls-concept:C0033268,
umls-concept:C0037083,
umls-concept:C0085862,
umls-concept:C0534519,
umls-concept:C0683598,
umls-concept:C1167395,
umls-concept:C1299583,
umls-concept:C1511545,
umls-concept:C1515655,
umls-concept:C1546856,
umls-concept:C1549571,
umls-concept:C1608386,
umls-concept:C1710082
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pubmed:issue |
7
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pubmed:dateCreated |
2010-3-22
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pubmed:abstractText |
To investigate the respective contributions of TLR versus IL-1R mediated signals in MyD88 dependent control of Mycobacterium tuberculosis, we compared the outcome of M. tuberculosis infection in MyD88, TRIF/MyD88, IL-1R1, and IL-1beta-deficient mice. All four strains displayed acute mortality with highly increased pulmonary bacterial burden suggesting a major role for IL-1beta signaling in determining the MyD88 dependent phenotype. Unexpectedly, the infected MyD88 and TRIF/MyD88-deficient mice, rather than being defective in IL-1beta expression, displayed increased cytokine levels relative to wild-type animals. Similarly, infected mice deficient in caspase-1 and ASC, which have critical functions in inflammasome-mediated IL-1beta maturation, showed unimpaired IL-1beta production and importantly, were considerably less susceptible to infection than IL-1beta deficient mice. Together our findings reveal a major role for IL-1beta in host resistance to M. tuberculosis and indicate that during this infection the cytokine can be generated by a mechanism that does not require TLR signaling or caspase-1.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1550-6606
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pubmed:author |
pubmed-author:BarberDaniel LDL,
pubmed-author:CasparPatriciaP,
pubmed-author:CheeverAllenA,
pubmed-author:FlavellRichard ARA,
pubmed-author:HienySaraS,
pubmed-author:KuglerDavidD,
pubmed-author:Mayer-BarberKatrin DKD,
pubmed-author:NúñezGabrielG,
pubmed-author:SchlueterDirkD,
pubmed-author:ShenderovKevinK,
pubmed-author:SherAlanA,
pubmed-author:SutterwalaFayyaz SFS,
pubmed-author:WhiteSandra DSD,
pubmed-author:WilsonMark SMS
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
184
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3326-30
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pubmed:meshHeading |
pubmed-meshheading:20200276-Adaptor Proteins, Vesicular Transport,
pubmed-meshheading:20200276-Animals,
pubmed-meshheading:20200276-Blotting, Western,
pubmed-meshheading:20200276-Caspase 1,
pubmed-meshheading:20200276-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:20200276-Female,
pubmed-meshheading:20200276-Interleukin-1beta,
pubmed-meshheading:20200276-Male,
pubmed-meshheading:20200276-Mice,
pubmed-meshheading:20200276-Mice, Inbred C57BL,
pubmed-meshheading:20200276-Mice, Transgenic,
pubmed-meshheading:20200276-Mycobacterium tuberculosis,
pubmed-meshheading:20200276-Myeloid Differentiation Factor 88,
pubmed-meshheading:20200276-Receptors, Interleukin-1,
pubmed-meshheading:20200276-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20200276-Signal Transduction,
pubmed-meshheading:20200276-Toll-Like Receptors,
pubmed-meshheading:20200276-Tuberculosis, Pulmonary
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pubmed:year |
2010
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pubmed:articleTitle |
Caspase-1 independent IL-1beta production is critical for host resistance to mycobacterium tuberculosis and does not require TLR signaling in vivo.
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pubmed:affiliation |
Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Intramural
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