PMID: 15240744Jul 9, 2004Paper

Chlamydia pneumoniae stimulates IFN-gamma synthesis through MyD88-dependent, TLR2- and TLR4-independent induction of IL-18 release

The Journal of Immunology : Official Journal of the American Association of Immunologists
Mihai G NeteaJos W M Van der Meer

Abstract

Recent studies suggest that inflammation plays a central role in the pathogenesis of atherosclerosis, and IFN-gamma is a prominent proinflammatory mediator in this context. However, it is unclear what stimuli are responsible for initial stimulation of IFN-gamma synthesis in the vessel wall. In the present study, we demonstrate that Chlamydia pneumoniae is an important stimulus for IFN-gamma synthesis, and this production depends on release of endogenous IL-18, IL-12, and IL-1, but not of TNF. The production of the proinflammatory cytokines TNF and IL-1beta from PBMC by sonicated C. pneumoniae was mediated through TLR2-dependent pathways. In contrast, C. pneumoniae stimulated the production of IL-18 through MyD88-dependent, TLR2-, TLR4-, and CD14-independent pathways, mediated by posttranscriptional mechanisms not involving de novo protein synthesis. In conclusion, C. pneumoniae is a potent stimulus of IFN-gamma production, in addition to the proinflammatory cytokines TNF and IL-1beta, which may contribute to its proatherogenic effects. Most interestingly, C. pneumoniae is also a potent inducer of IL-18 production through pathways independent of TLR2 and TLR4.

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Citations

Mar 16, 2007·Journal of Leukocyte Biology·Christian TrumstedtMartin E Rottenberg
Feb 10, 2007·American Journal of Respiratory and Critical Care Medicine·Daniel DroemannKlaus Dalhoff
Apr 13, 2006·European Journal of Immunology·Nuria RodriguezThomas Miethke
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Jun 8, 2021·Frontiers in Immunology·Wenjing XiangZhou Zhou
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