Linked Life Data

11943771

Source:http://linkedlifedata.com/resource/pubmed/id/11943771

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
35
pubmed:dateCreated
2002-8-30
pubmed:abstractText
Bacterial lipopolysaccharide (LPS) evokes several functional responses in the neutrophil that contribute to innate immunity. Although certain responses, such as adhesion and synthesis of tumor necrosis factor-alpha, are inhibited by pretreatment with an inhibitor of p38 mitogen-activated protein kinase, others, such as actin assembly, are unaffected. The aim of the present study was to investigate the changes in neutrophil gene transcription and protein expression following lipopolysaccharide exposure and to establish their dependence on p38 signaling. Microarray analysis indicated expression of 13% of the 7070 Affymetrix gene set in nonstimulated neutrophils, and LPS up-regulation of 100 distinct genes, including cytokines and chemokines, signaling molecules, and regulators of transcription. Proteomic analysis yielded a separate list of up-regulated modulators of inflammation, signaling molecules, and cytoskeletal proteins. Poor concordance between mRNA transcript and protein expression changes was noted. Pretreatment with the p38 inhibitor SB203580 attenuated 23% of LPS-regulated genes and 18% of LPS-regulated proteins by > or = 40%. This study indicates that p38 plays a selective role in regulation of neutrophil transcripts and proteins following lipopolysaccharide exposure, clarifies that several of the effects of lipopolysaccharide are post-transcriptional and post-translational, and identifies several proteins not previously reported to be involved in the innate immune response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31291-302
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11943771-Amino Acid Sequence, pubmed-meshheading:11943771-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:11943771-Electrophoresis, Gel, Two-Dimensional, pubmed-meshheading:11943771-Gene Expression Regulation, Enzymologic, pubmed-meshheading:11943771-Humans, pubmed-meshheading:11943771-Imidazoles, pubmed-meshheading:11943771-Lipopolysaccharides, pubmed-meshheading:11943771-Mitogen-Activated Protein Kinases, pubmed-meshheading:11943771-Neutrophils, pubmed-meshheading:11943771-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:11943771-Proteome, pubmed-meshheading:11943771-Pyridines, pubmed-meshheading:11943771-RNA, Messenger, pubmed-meshheading:11943771-Recombinant Proteins, pubmed-meshheading:11943771-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11943771-Spectrometry, Mass, Matrix-Assisted Laser..., pubmed-meshheading:11943771-Transcription, Genetic, pubmed-meshheading:11943771-p38 Mitogen-Activated Protein Kinases
pubmed:year
2002
pubmed:articleTitle
A genomic and proteomic analysis of activation of the human neutrophil by lipopolysaccharide and its mediation by p38 mitogen-activated protein kinase.
pubmed:affiliation
Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center and National Jewish Medical and Research Center, Denver, Colorado 80262, USA.
pubmed:publicationType
Journal Article