Linked Life Data

17114467

Source:http://linkedlifedata.com/resource/pubmed/id/17114467

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2006-11-20
pubmed:abstractText
Helicobacter pylori infection is associated with the local production of chemokines and cytokines, of which IL-6 is overexpressed at the margin of gastric ulcer in H. pylori-positive gastritis. Cells of the monocytic lineage are the major sources of IL-6, and mononuclear cell infiltration in the lamina propria is characteristic of H. pylori-induced chronic infection. Our study shows for the first time that a secreted peptidyl prolyl cis-, trans-isomerase, HP0175 elicits IL-6 gene expression and IL-6 release from macrophages. An isogenic strain inactivated in the HP0175 gene (knockout) was attenuated in its IL-6-inducing ability, which was restored after complementation with the HP0175 gene. The specificity of the HP0175-induced effect was confirmed by the fact that rHP0175 purified from HEK293 cells could also induce IL-6 release, ruling out the possibility that the observed effect was due to bacterial contaminants. HP0175 was capable of interacting directly with the extracellular domain of TLR4. HP0175-induced IL-6 gene expression was critically dependent on TLR4-dependent NF-kappaB and MAPK activation. TLR4/PI3K-dependent ERK1/2 and p38 MAPK signaling converged upon activation of mitogen- and stress-activated protein kinase 1 (MSK1). The central role of MSK1 was borne out by the fact that silencing of MSK1 expression abrogated HP0175-mediated NF-kappaB-dependent IL-6 gene transcription. MSK1 regulated the recruitment of p65 and phopho-Ser(10)-histone H3 to the IL-6 promoter. HP0175 therefore regulated IL-6 gene transcription through chromatin modification at the IL-6 promoter.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7950-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17114467-Blotting, Western, pubmed-meshheading:17114467-Cells, Cultured, pubmed-meshheading:17114467-Enzyme Activation, pubmed-meshheading:17114467-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:17114467-Gene Expression, pubmed-meshheading:17114467-Helicobacter pylori, pubmed-meshheading:17114467-Humans, pubmed-meshheading:17114467-Interleukin-6, pubmed-meshheading:17114467-Macrophages, pubmed-meshheading:17114467-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:17114467-Mitogen-Activated Protein Kinase 8, pubmed-meshheading:17114467-Mitogen-Activated Protein Kinases, pubmed-meshheading:17114467-NF-kappa B, pubmed-meshheading:17114467-Peptidylprolyl Isomerase, pubmed-meshheading:17114467-Phosphorylation, pubmed-meshheading:17114467-RNA, Small Interfering, pubmed-meshheading:17114467-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:17114467-Signal Transduction, pubmed-meshheading:17114467-Toll-Like Receptor 4
pubmed:year
2006
pubmed:articleTitle
TLR4-dependent NF-kappaB activation and mitogen- and stress-activated protein kinase 1-triggered phosphorylation events are central to Helicobacter pylori peptidyl prolyl cis-, trans-isomerase (HP0175)-mediated induction of IL-6 release from macrophages.
pubmed:affiliation
Department of Chemistry, Bose Institute, 93/1 Acharya Prafulla, Chandra Road, Kolkata 700009, India.
pubmed:publicationType
Journal Article