Abstract:
:Accumulating evidence suggest that infection with Chlamydia pneumoniae is associated with atherosclerosis, but the mechanisms involved remain unclear. Inflammation is important in the initial phase of atherogenesis, and cytokines are important in the initiation and progression of inflammation. The aim of this study was to assess the capacity of acellular components of C. pneumoniae to stimulate the production of pro-inflammatory cytokines and chemokines. Peripheral blood mononuclear cells were stimulated in vitro with sonicated C. pneumoniae. Significant amounts of TNF-alpha, IL-1, IL-6, IL-8, monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha (MIP-1alpha) were produced. Inhibition of endotoxin using polymyxin B revealed that chlamydial endotoxin plays a minor role in the cytokine induction. Neutralization of TNF by TNF-binding protein and blockade of IL-1 receptors by IL-1 receptor antagonist revealed that TNF, IL-1 and IL-6 production was independent from each other, whereas IL-8 synthesis was strongly dependent on endogenous TNF and IL-1. In contrast, synthesis of MCP-1 and MIP-1alpha was dependent on endogenous TNF, but not IL-1. In conclusion, acellular components of C. pneumoniae are a potent stimulus for cytokine production, and this mechanism may have an important role in the inflammatory aspects of atherogenesis.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Netea MG,Selzman CH,Kullberg BJ,Galama JM,Weinberg A,Stalenhoef AF,Van der Meer JW,Dinarello CAdoi
10.1002/1521-4141(200002)30:2<541::AID-IMMU541>3.0keywords:
subject
Has Abstractpub_date
2000-02-01 00:00:00pages
541-9issue
2eissn
0014-2980issn
1521-4141pii
10.1002/(SICI)1521-4141(200002)30:02<541::AID-IMMUjournal_volume
30pub_type
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