Nuclear Factor–κB Activation in Endothelium by Chlamydia pneumoniae without Active Infection
Causative molecular mechanisms accounting for the potential link between Chlamydia pneumoniae and atherosclerosis are unknown. Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear factor (NF)–κB in cultured porcine endothelium and up-regulated the expression of E-se...
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| Veröffentlicht in: | The Journal of infectious diseases 2003-10, Vol.188 (8), p.1094-1097 |
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| container_end_page | 1097 |
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| container_issue | 8 |
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| container_title | The Journal of infectious diseases |
| container_volume | 188 |
| creator | Baer, Jefferson T. du Laney, Tracey V. Wyrick, Priscilla B. McCain, Arlene S. Fischer, Thomas A. Merricks, Elizabeth P. Baldwin, Albert S. Nichols, Timothy C. |
| description | Causative molecular mechanisms accounting for the potential link between Chlamydia pneumoniae and atherosclerosis are unknown. Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear factor (NF)–κB in cultured porcine endothelium and up-regulated the expression of E-selectin messenger RNA and protein. This up-regulation was abolished by an IκB super-repressor, an NF-κB–specific inhibitor. Live bacteria are not necessary for the activation of endothelial NF-κB, and C. pneumoniae may contribute to atherogenesis without active infection |
| doi_str_mv | 10.1086/378564 |
| format | Article |
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Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear factor (NF)–κB in cultured porcine endothelium and up-regulated the expression of E-selectin messenger RNA and protein. This up-regulation was abolished by an IκB super-repressor, an NF-κB–specific inhibitor. 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Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear factor (NF)–κB in cultured porcine endothelium and up-regulated the expression of E-selectin messenger RNA and protein. This up-regulation was abolished by an IκB super-repressor, an NF-κB–specific inhibitor. 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Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear factor (NF)–κB in cultured porcine endothelium and up-regulated the expression of E-selectin messenger RNA and protein. This up-regulation was abolished by an IκB super-repressor, an NF-κB–specific inhibitor. Live bacteria are not necessary for the activation of endothelial NF-κB, and C. pneumoniae may contribute to atherogenesis without active infection</abstract><pub>The University of Chicago Press</pub><doi>10.1086/378564</doi><tpages>4</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | The Journal of infectious diseases, 2003-10, Vol.188 (8), p.1094-1097 |
| issn | 0022-1899 1537-6613 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_19156866 |
| source | Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection; JSTOR |
| subjects | Chlamydia pneumoniae E-selectin |
| title | Nuclear Factor–κB Activation in Endothelium by Chlamydia pneumoniae without Active Infection |
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