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Synthesis through MyD88-Dependent, TLR2- and TLR4-Independent Induction of IL-18 Release1
,
Departments of
*
Medicine and
Medical Microbiology, University Medical Center Nijmegen, and
Nijmegen University Center for Infectious Diseases, Nijmegen, The Netherlands; and
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO
Recent studies suggest that inflammation plays a central role in the pathogenesis of atherosclerosis, and IFN-
is a prominent proinflammatory mediator in this context. However, it is unclear what stimuli are responsible for initial stimulation of IFN- synthesis in the vessel wall. In the present study, we demonstrate that Chlamydia pneumoniae is an important stimulus for IFN- 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-1
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- production, in addition to the proinflammatory cytokines TNF and IL-1, 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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