Abstract:
:Strong sero-epidemiologic, pathologic, and experimental evidence suggests that Chlamydophila pneumoniae (Cpn) infection may play a causative role in the development of atherosclerosis. Cpn is an obligate intracellular gram-negative bacterium that is responsible for 10% of cases of community-acquired pneumonia. In addition to its presence in the respiratory tract, live Cpn has been found within atherosclerotic plaques. Experimental findings have established Cpn's ability to infect vascular cells and elicit important atherogenic responses. Furthermore, Cpn infection can promote atherosclerotic development in different animal models. To date however, large-scale antibiotic clinical trials have not been effective in preventing major cardiovascular events. It is becoming apparent that Cpn undergoes a persistent state of infection, which is refractory to current chlamydial antibiotics. New treatment strategies that are effective toward acute and persistent forms of Cpn infection are needed in order to effectively eradicate the bacterium within the vascular wall. Possible therapeutics targets include Cpn-specific proteins and machinery directly involved in their survival, replication and maintenance. Alternatively, selectively targeting host cell pathways and machinery required for Cpn's actions in vascular cells also represent potential treatment strategies for atherosclerosis.
journal_name
Fundam Clin Pharmacoljournal_title
Fundamental & clinical pharmacologyauthors
Deniset JF,Pierce GNdoi
10.1111/j.1472-8206.2010.00863.xsubject
Has Abstractpub_date
2010-10-01 00:00:00pages
607-17issue
5eissn
0767-3981issn
1472-8206pii
FCP863journal_volume
24pub_type
杂志文章,评审abstract::An antagonism between cholecystokinin (CCK) peptides and benzodiazepines (BZD) has been described in various paradigms. We sought to determine whether CCK and BZD are also antagonistic in their effects on brain neurotransmitter levels in the rat. No effect on the noradrenergic system was induced in any brain area by C...
journal_title:Fundamental & clinical pharmacology
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doi:10.1111/j.1472-8206.1990.tb00491.x
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
pub_type: 杂志文章,随机对照试验
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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更新日期:2003-06-01 00:00:00
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journal_title:Fundamental & clinical pharmacology
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pub_type: 临床试验,杂志文章,随机对照试验
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
pub_type: 杂志文章,随机对照试验
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journal_title:Fundamental & clinical pharmacology
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