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

Vera M. Ripoll, Aras Kadioglu, Roger Cox, David A. Hume, Paul Denny

Research output: Contribution to journalArticlepeer-review

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-κB, and ERK 1/2 signaling pathways, resulting in reduced secretion of TNF-α 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.
Original languageEnglish
Pages (from-to)735-741
Number of pages7
JournalJournal of Leukocyte Biology
Volume87
Issue number4
DOIs
Publication statusPublished - Apr 2010

Keywords

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

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