Endothelial Dysfunction After Repeated
            <i>Chlamydia pneumoniae</i>
            Infection in Apolipoprotein E–Knockout Mice

Liuba, Petru; Karnani, Päivi; Pesonen, Erkki; Paakkari, Ilari; Forslid, A.; Johansson, Leif; Persson, Kenneth; Wadström, Torkel; Laurini, Ricardo

doi:10.1161/01.cir.102.9.1039

Cited by 94 publications

(70 citation statements)

References 40 publications

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“…This could increase the proteolytic and cytotoxic activity in the plaque, perhaps leading to plaque rupture and myocardial ischemia. In addition, CP may hamper endothelial NO production 22 ; this might increase the risk for vasospastic events and precipitate myocardial infarction. Thus, CP could be important for ischemia in the atherosclerotic heart rather than accelerating the early phase of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Chlamydia pneumoniae Infection Does Not Induce or Modify Atherosclerosis in Mice

et al. 2001

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Background-Seroepidemiological studies have linked Chlamydia pneumoniae (CP) to coronary heart disease, and recent experimental studies suggest that it may accelerate or even induce atherosclerosis. We therefore evaluated the effect of CP infection on atherosclerosis in atherosclerosis-prone apolipoprotein E-knockout (apoE-KO) and wild-type C57BL/6J mice. Methods and Results-Six-to 8-week-old female mice were infected intranasally with live CP and then fed a standard chow diet for 22 weeks. A subgroup of mice was reinfected 18 weeks after primary infection. Polymerase chain reaction analysis of lung tissue confirmed successful infection with CP, and ELISA assays demonstrated development of a humoral immune response. Despite this, no statistically significant differences in aortic atherosclerotic lesions were found between CP-infected and control apoE-KO mice. Furthermore, CP infection did not induce atherosclerosis in C57BL/6J mice. Conclusions-CP does not induce atherosclerosis in wild-type mice and does not accelerate atherosclerosis in chow-fed apoE-KO mice. Further studies will be necessary to clarify the explanation for the seroepidemiological association between CP and coronary heart disease in humans.

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Section: Discussionmentioning

confidence: 99%

Chlamydia pneumoniae Infection Does Not Induce or Modify Atherosclerosis in Mice

et al. 2001

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“…Infectious pathogens initiate endothelial damage [22,24]. Acute infections worsen the endothelial cell function which might not have returned quite normal even after one year [25].…”

Section: Mechanism Of Infection Initiated Chdmentioning

confidence: 99%

Dual role of infections as risk factors for coronary heart disease

et al. 2007

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“…C. pneumoniae has been suggested to accelerate endothelial inflammation and therefore promoting vascular diseases (68), and indeed, C. pneumoniae infection of endothelial cells has been demonstrated to induce the release of chemoattractants, proinflammatory cytokines, and myeloid growth factors (44,69), cytokines that are also thought to be involved in atherosclerosis (70)(71)(72)(73). Activation of IRF3 has recently been linked to the development of atherosclerosis by mediating defects in cholesterol clearance (74).…”

Section: Discussionmentioning

confidence: 99%

Essential Role of Mitochondrial Antiviral Signaling, IFN Regulatory Factor (IRF)3, and IRF7 in Chlamydophila pneumoniae-Mediated IFN-β Response and Control of Bacterial Replication in Human Endothelial Cells

Buß

Opitz

Hocke

et al. 2010

The Journal of Immunology

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Chlamydophila pneumoniae infection of the vascular wall as well as activation of the transcription factor IFN regulatory factor (IRF)3 have been linked to development of chronic vascular lesions and atherosclerosis. The innate immune system detects invading pathogens by use of pattern recognition receptors, some of which are able to stimulate IRF3/7 activation and subsequent type I IFN production (e. g., IFN-β). In this study, we show that infection of human endothelial cells with C. pneumoniae-induced production of IFN-β, a cytokine that so far has been mainly associated with antiviral immunity. Moreover, C. pneumoniae infection led to IRF3 and IRF7 nuclear translocation in HUVECs and RNA interference experiments showed that IRF3 and IRF7 as well as the mitochondrial antiviral signaling (MAVS) were essential for IFN-β induction. Finally, C. pneumoniae replication was enhanced in endothelial cells in which IRF3, IRF7, or MAVS expression was inhibited by small interfering RNA and attenuated by IFN-β treatment. In conclusion, C. pneumoniae infection of endothelial cells activates an MAVS-, IRF3-, and IRF7-dependent signaling, which controls bacterial growth and might modulate development of vascular lesions.

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Endothelial Dysfunction After Repeated Chlamydia pneumoniae Infection in Apolipoprotein E–Knockout Mice

Cited by 94 publications

References 40 publications

Chlamydia pneumoniae Infection Does Not Induce or Modify Atherosclerosis in Mice

Chlamydia pneumoniae Infection Does Not Induce or Modify Atherosclerosis in Mice

Dual role of infections as risk factors for coronary heart disease

Essential Role of Mitochondrial Antiviral Signaling, IFN Regulatory Factor (IRF)3, and IRF7 in Chlamydophila pneumoniae-Mediated IFN-β Response and Control of Bacterial Replication in Human Endothelial Cells

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