rdf:type |
|
lifeskim:mentions |
umls-concept:C0023810,
umls-concept:C0024320,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0035820,
umls-concept:C0079189,
umls-concept:C0206527,
umls-concept:C0330390,
umls-concept:C0521009,
umls-concept:C1158770,
umls-concept:C1519477
|
pubmed:issue |
12
|
pubmed:dateCreated |
1999-4-5
|
pubmed:abstractText |
Lymphotoxin alpha (LT-alpha) and lymphotoxin beta (LT-beta) are members of the tumour necrosis factor (TNF) ligand family. Because of the importance of TNF in the pathogenesis of septic shock, the expression of LT-alpha and LT-beta mRNA in murine splenocytes stimulated with different pro-inflammatory cytokines, sepsis-associated mediators such as lipopolysaccharide (LPS) and bacterial superantigens was investigated. The authors show that the bacterial superantigens, toxic shock syndrome toxin 1 (TSST-1) and staphylococcal enterotoxin B (SEB) upregulate LT-alpha mRNA expression in vitro in murine cells. Basal expression of LT-beta mRNA was found in unstimulated murine splenocytes, and could be increased by the addition of the mitogen concanavalin A (Con A). Despite this suggested inducibility of the murine LT-beta transcript, sepsis-associated mediators did not affect its regulation. Neither the pro-inflammatory cytokines interleukin 2 (IL-2), TNF-alpha nor LPS alone or in combination with interferon gamma (IFN-gamma) had any effect on LT-beta mRNA expression. The bacterial superantigens TSST-1, SEB and streptococcal pyrogenic exotoxin A (SPEA) were also unable to upregulate LT-beta mRNA transcript, in contrast to the observation with LT-alpha.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Concanavalin A,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Ltb protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphotoxin-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphotoxin-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Superantigens
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
|
pubmed:issn |
1043-4666
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pubmed:author |
|
pubmed:copyrightInfo |
Copyright 1998 Academic Press.
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pubmed:issnType |
Print
|
pubmed:volume |
10
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
940-7
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:10049517-Aging,
pubmed-meshheading:10049517-Animals,
pubmed-meshheading:10049517-Base Sequence,
pubmed-meshheading:10049517-Concanavalin A,
pubmed-meshheading:10049517-Cytokines,
pubmed-meshheading:10049517-DNA Primers,
pubmed-meshheading:10049517-Inflammation Mediators,
pubmed-meshheading:10049517-Lipopolysaccharides,
pubmed-meshheading:10049517-Lymphotoxin-alpha,
pubmed-meshheading:10049517-Lymphotoxin-beta,
pubmed-meshheading:10049517-Membrane Proteins,
pubmed-meshheading:10049517-Mice,
pubmed-meshheading:10049517-Mice, Inbred BALB C,
pubmed-meshheading:10049517-RNA, Messenger,
pubmed-meshheading:10049517-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:10049517-Sepsis,
pubmed-meshheading:10049517-Spleen,
pubmed-meshheading:10049517-Superantigens,
pubmed-meshheading:10049517-Transcription, Genetic,
pubmed-meshheading:10049517-Up-Regulation
|
pubmed:year |
1998
|
pubmed:articleTitle |
The role of lipopolysaccharide, pro-inflammatory cytokines and bacterial superantigens in the transcriptional regulation of lymphotoxin alpha and beta in mouse splenocytes.
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pubmed:affiliation |
Department of Infectious Diseases, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|