Lars Jørgen Østergaard

Streptococcus pneumoniae stabilizes tumor necrosis factor alpha mRNA through a pathway dependent on p38 MAPK but independent of Toll-like receptors.

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  • The Department of Infectious Diseases
  • Department of Medical Microbiology and Immunology
ABSTRACT: BACKGROUND: Streptococcus pneumoniae is a human pathogenic bacteria and a major cause of severe invasive diseases, including pneumonia, bacteraemia, and meningitis. Infections with S. pneumoniae evoke a strong inflammatory response, which plays a major role in the pathogenesis of pneumococcal disease. RESULTS: In this study, we have examined how S. pneumoniae affects expression of the inflammatory cytokine tumor necrosis factor (TNF) alpha, and the molecular mechanisms involved. Production of TNF-alpha protein was strongly induced by S. pneumoniae, which was able to stabilize TNF-alpha mRNA, through a mechanism dependent on the viability of the bacteria as well as the AU-rich elements in the 3' untranslated region of TNF-alpha mRNA. The ability of S. pneumoniae to stabilize TNF-alpha mRNA was dependent on the mitogen-activated protein kinase p38, whereas inhibition of Toll-like receptor signaling did not affect S. pneumoniae-induced mRNA stabilization. CONCLUSIONS: Thus, S. pneumoniae stabilizes TNF-alpha mRNA through a pathway dependent on p38 but independent of Toll-like receptors.
Original languageEnglish
JournalB M C Immunology
Pages (from-to)52
Publication statusPublished - 2008

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