Modulated by Liver X Receptor Activation -Independent Signaling and Is Reciprocally Formation Requires MyD88-Dependent and -Induced Foam Cell Chlamydia pneumoniae

نویسندگان

  • Moshe Arditi
  • Yonca Bulut
  • Terence M. Doherty
  • Timothy R. Crother
  • Shuang Chen
  • Rosalinda Sorrentino
  • Kenichi Shimada
چکیده

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TLR/MyD88 and liver X receptor alpha signaling pathways reciprocally control Chlamydia pneumoniae-induced acceleration of atherosclerosis.

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Intracellular Bacterial Infection-Induced IFN- Is Critically but Not Solely Dependent on Toll-Like Receptor 4-Myeloid Differentiation Factor 88-IFN- -STAT1 Signaling

Infection of murine bone marrow-derived macrophages (BMM ) with Chlamydia pneumoniae induces IFN-dependent IFNsecretion that leads to control of the intracellular bacterial growth. Enhanced growth of C. pneumoniae in Toll-like receptor (TLR) 4 / and myeloid differentiation factor (MyD) 88 / (but not TLR2 / , TLR6 / , or TLR9 / ) BMM is shown in this study. Reduced accumulation of IFNand IFNmRNA...

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Decreased expression of liver X receptor-α in macrophages infected with Chlamydia pneumoniae in human atherosclerotic arteries in situ.

In in vitro experiments, Chlamydia pneumoniae has been shown to infect macrophages and to accelerate foam cell formation. It has been hypothesized that the C. pneumoniae infection affects foam cell formation by suppressing the expression of liver X receptors (LXR), but whether such an event occurs in human atherosclerosis is not known. In this study we examined carotid artery segments, obtained...

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A Chlamydia pneumoniae component that induces macrophage foam cell formation is chlamydial lipopolysaccharide.

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تاریخ انتشار 2008