Source:http://linkedlifedata.com/resource/pubmed/id/11911801
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
2002-3-25
|
pubmed:abstractText |
CXC chemokine-interleukin-8 (IL-8) (CXCL-8) is a potent proinflammatory chemotactic factor that induces important immune responses for antimycobacterial defenses. However, little is known about the biochemical mechanisms by which the mycobacterial antigens upregulate the release of CXCL-8 from human monocytes. In this study, the mechanisms through which Mycobacterium bovis BCG induces CXCL-8 secretion in human monocytes were investigated. We found that M. bovis BCG induced the production of high levels of CXCL-8 by human monocytes. M. bovis-induced CXCL-8 secretion was unaffected by the protein kinase C (PKC) inhibitor bisindolylmaleimide. In contrast, preincubation of the monocytes with the protein tyrosine kinase (PTK) inhibitor genistein resulted in dose-dependent suppression of mycobacteria-induced CXCL-8 secretion. These results were further supported by the fact that treatment of monocytes with herbimycin-A, another well-described inhibitor of PTK activity with a different mechanism of action, significantly diminished the effect of M. bovis on CXCL-8 secretion. In addition, the specificity of this inhibition was demonstrated by the inability of herbimycin-A to block in a significant manner IL-1 beta induction of CXCL-8. Herbimycin-A significantly blocked tyrosine phosphorylation of p59(hck) in response to M. bovis. Finally, two specific NF-kappa B inhibitors, sulfasalazine and caffeic acid phenetyl ester (CAPE), strongly inhibited the production of CXCL-8 by human monocytes infected with M. bovis. These results show intracellular signaling pathways and a transcription factor involved in the M. bovis-mediated upregulation of CXCL-8 biosynthesis and release by human monocytes.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents...,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Genistein,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfasalazine
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
1079-9907
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
22
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
189-97
|
pubmed:dateRevised |
2009-11-19
|
pubmed:meshHeading |
pubmed-meshheading:11911801-Anti-Inflammatory Agents, Non-Steroidal,
pubmed-meshheading:11911801-Cells, Cultured,
pubmed-meshheading:11911801-Enzyme Inhibitors,
pubmed-meshheading:11911801-Genistein,
pubmed-meshheading:11911801-Humans,
pubmed-meshheading:11911801-Interleukin-8,
pubmed-meshheading:11911801-Monocytes,
pubmed-meshheading:11911801-Mycobacterium bovis,
pubmed-meshheading:11911801-NF-kappa B,
pubmed-meshheading:11911801-Protein-Tyrosine Kinases,
pubmed-meshheading:11911801-Signal Transduction,
pubmed-meshheading:11911801-Sulfasalazine
|
pubmed:year |
2002
|
pubmed:articleTitle |
Signals involved in mycobacteria-induced CXCL-8 production by human monocytes.
|
pubmed:affiliation |
Departamento de Immunologia, Escuela Nacional de Ciencias Biológicas, IPN, Carpio y Plan de Ayala, México, D.F. 11340 México. pmendezs@bios.encb.ipn.mx
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|