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We tested whether polymorphic membrane proteins (PMPs) of Chlamydia pneumoniae might play a role in triggering an inflammatory response in human endothelial cells. Of 15 purified, recombinant chlamydial PMPs tested, 2 (PMP 20 and PMP 21) dose-dependently increased the production of the inflammatory mediators interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1), in cultured human endothelial cells; production of IL-8 was also increased. When endothelial cells were infected by live C. pneumoniae, an increase in the production of IL-6, IL-8, and MCP-1 was seen. We used adenovirus-induced overexpression of IkappaBalpha-an inhibitor of nuclear factor (NF)-kappaB-to demonstrate that PMP 20 and PMP 21 increase the production of IL-6 and MCP-1 in human endothelial cells by activation of the NF-kappaB pathway, because, in cells overexpressing IkappaBalpha, treatment with the respective PMP did not result in increased production of IL-6 and MCP-1. Thus, C. pneumoniae could, by interactions of its PMPs with the endothelium, contribute to the process of vascular injury during the development and progression of atherosclerotic lesions.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Polymorphic Membrane Protein (PMP) 20 and PMP 21 of<i>Chlamydia pneumoniae</i>Induce Proinflammatory Mediators in Human Endothelial Cells In Vitro by Activation of the Nuclear Factor‐κB Pathway

Polymorphic Membrane Protein (PMP) 20 and PMP 21 ofChlamydia pneumoniaeInduce Proinflammatory Mediators in Human Endothelial Cells In Vitro by Activation of the Nuclear Factor‐κB Pathway