Wednesday, 28 April 2010

What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2010 Apr 28
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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PubMed Results
Item 1 of 1

1. J Leukoc Biol. 2010 Apr;87(4):735-41. Epub 2009 Dec 22.

Macrophages from BALB/c and CBA/Ca mice differ in their cellular responses to Streptococcus pneumoniae.

Ripoll VM, Kadioglu A, Cox R, Hume DA, Denny P.

Mammalian Genetics Unit, Medical Research Council, Harwell, Oxfordshire OX11 0RD, UK. v.ripoll@har.mrc.ac.uk

Abstract

In a mouse model of pneumonia caused by Streptococcus pneumoniae, differences in the timing and vigor of the host inflammatory response have been associated with susceptibility to invasive disease. BALB/c and CBA/Ca mice are known to be resistant and susceptible to acute pneumococcal disease, respectively. In this study, we have demonstrated that BMM from BALB/c and CBA/Ca mice differ in their expression and regulation of TLR9 in response to S. pneumoniae. We have also shown that BMM from CBA/Ca mice failed to fully activate p38, NF-kappaB, and ERK 1/2 signaling pathways, resulting in reduced secretion of TNF-alpha and CCL5 in response to this pathogen. In addition, we have established that S. pneumoniae induced significant cell death in BMM from CBA/Ca mice. These findings indicate that variations between the two strains are likely to reflect differences in macrophage responses to the pathogen.

PMID: 20028774 [PubMed - indexed for MEDLINE]
Click here to read

MeSH Terms:

  • Acute Disease
  • Animals
  • Cell Death/immunology
  • Chemokine CCL5/immunology
  • Chemokine CCL5/metabolism
  • Disease Models, Animal
  • Inflammation/immunology
  • Inflammation/metabolism
  • MAP Kinase Signaling System/immunology*
  • Macrophages/immunology*
  • Macrophages/metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mitogen-Activated Protein Kinase 3/immunology
  • Mitogen-Activated Protein Kinase 3/metabolism
  • NF-kappa B/immunology
  • NF-kappa B/metabolism
  • Pneumonia, Pneumococcal/immunology*
  • Pneumonia, Pneumococcal/metabolism
  • Species Specificity
  • Streptococcus pneumoniae/immunology*
  • Streptococcus pneumoniae/metabolism
  • Toll-Like Receptor 9/biosynthesis
  • Toll-Like Receptor 9/immunology
  • Tumor Necrosis Factor-alpha/immunology
  • Tumor Necrosis Factor-alpha/secretion
  • p38 Mitogen-Activated Protein Kinases/immunology
  • p38 Mitogen-Activated Protein Kinases/metabolism

Substances:

  • Ccl5 protein, mouse
  • Chemokine CCL5
  • NF-kappa B
  • Tlr9 protein, mouse
  • Toll-Like Receptor 9
  • Tumor Necrosis Factor-alpha
  • Mitogen-Activated Protein Kinase 3
  • p38 Mitogen-Activated Protein Kinases

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