Linked Life Data

11046047

Source:http://linkedlifedata.com/resource/pubmed/id/11046047

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2000-11-3
pubmed:abstractText
The immunomodulatory role of unmethylated cytosine-guanine sequences (CpG) in bacterial DNA has been well documented. We have previously demonstrated that murine macrophage-like RAW 264.7 cells respond to CpG DNA with an increase in the proinflammatory cytokine, TNF-alpha, in both a dose-dependent and time-dependent manner. In addition, CpG DNA stimulates a significant, though delayed, secretion of the anti-inflammatory cytokine IL-10. Because TNF-alpha and TNFR (TNFRI and II) expression are tightly regulated responses, we hypothesized that CpG containing oligodeoxynucleotide (CpG ODN) would also affect TNFRI and II shedding. Using both murine peritoneal macrophages and RAW 264.7 cells, we demonstrated a significant, time-dependent increase in soluble TNFRI and TNFRII production with CpG ODN stimulation. RAW 264.7 cells treated with CpG ODN had a transient increase in membrane TNFRII expression, but not TNFRI. Both types of TNFR mRNA were also up-regulated by CpG ODN, and addition of the transcriptional inhibitor actinomycin D abrogated the effect of CpG ODN on TNFR mRNA and protein expression. Addition of anti-IL-10 and anti-TNF-alpha Abs did not change these results. The addition of plate-bound anti-TNF receptor Abs to this system increased the amount of bioactive TNF, implying that these receptors are acting as inhibitors of TNF activity. These results suggest that the de novo, non-IL-10- and non-TNF-alpha-dependent transcription, translation, and shedding of TNFRs are additional potential counterinflammatory effects of CpG DNA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5153-60
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11046047-Adjuvants, Immunologic, pubmed-meshheading:11046047-Animals, pubmed-meshheading:11046047-Antigens, CD, pubmed-meshheading:11046047-Cell Line, pubmed-meshheading:11046047-CpG Islands, pubmed-meshheading:11046047-Female, pubmed-meshheading:11046047-Interleukin-10, pubmed-meshheading:11046047-Macrophages, Peritoneal, pubmed-meshheading:11046047-Mice, pubmed-meshheading:11046047-Mice, Inbred BALB C, pubmed-meshheading:11046047-Oligodeoxyribonucleotides, pubmed-meshheading:11046047-RNA, Messenger, pubmed-meshheading:11046047-Receptors, Tumor Necrosis Factor, pubmed-meshheading:11046047-Receptors, Tumor Necrosis Factor, Type I, pubmed-meshheading:11046047-Receptors, Tumor Necrosis Factor, Type II, pubmed-meshheading:11046047-Solubility, pubmed-meshheading:11046047-Tumor Necrosis Factor-alpha, pubmed-meshheading:11046047-Up-Regulation
pubmed:year
2000
pubmed:articleTitle
Enhanced murine macrophage TNF receptor shedding by cytosine-guanine sequences in oligodeoxynucleotides.
pubmed:affiliation
Surgical Infectious Disease Laboratory, Department of Surgery, and Department of Internal Medicine, University of Virginia, Charlottesville, VA 22906, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.