<i>Chlamydia Pneumoniae</i>
            , Cytomegalovirus, and Herpes Simplex Virus in Atherosclerosis of the Carotid Artery

Chiu, Brian; Viira, Esther; Tucker, William S.; Fong, I. W.

doi:10.1161/01.cir.96.7.2144

Cited by 295 publications

(200 citation statements)

References 25 publications

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“…29,30 In addition, TLR9 expressed by pDCs may recognize endogenous danger signals in the atherosclerotic plaque. In particular, self-DNA is able to trigger pDCs via TLR9.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

et al. 2007

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“…29,30 In addition, TLR9 expressed by pDCs may recognize endogenous danger signals in the atherosclerotic plaque. In particular, self-DNA is able to trigger pDCs via TLR9.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

et al. 2007

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“…34 Also, it can still be argued that viral infections, not affected by macrolide treatment, are involved in atherogenesis, arterial thrombosis and plaque rupture. 35,36 Recently, Ad infections were considered to play a role in the development of obesity and are associated with plasma lipid abnormalities. 15,17,18,37,38 In the present study it is shown that a range of different viral and bacterial microorganisms are able to infect human adipocytes and induce an inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Infection-induced inflammatory response of adipocytes in vitro

et al. 2008

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Background: Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Methods: Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Results: Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192 ± 22 pg ml À1 (uninfected) to 1030 ± 86 pg ml À1 , 838 ± 59 pg ml À1 and 1241 ± 191 pg ml À1 , respectively (all Po0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285 ± 26.8 ng ml À1 vs uninfected: 477 ± 71.2 ng ml À1 ; P ¼ 0.05) and pre-adipocytes (709±43.3 ng ml À1 vs uninfected: 1071±71.8 ng ml À1 ; Po0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF-a production. Conclusions: Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes.

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“…Epidemiological data (9)(10)(11)28) indicate the frequent infection of arteries with microbial pathogens. It is conceivable that successful immune responses against these pathogens are crucial to limit direct cytopathic and indirect immunopathological damage during vascular infections.…”

Section: Mutual Chronic Perpetuation Of Vascular Inflammation and Chomentioning

confidence: 99%

“…In humans, herpesvirus DNA or antigen can be found in atherosclerotic lesions in patients with coronary artery disease (9,10). In addition, there is a correlation between seroreactivity against Chlamydia pneumoniae and coronary heart disease (11), and C. pneunoniae antigen can be detected in patients with carotid artery stenosis (10).…”

mentioning

confidence: 99%

Linking immune-mediated arterial inflammation and cholesterol-induced atherosclerosis in a transgenic mouse model

Ludewig

Freigang

Jäggi

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

128

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Arterial inflammatory responses are thought to be a significant component of atherosclerotic disease. We describe here, using a transgenic approach, the mutual perpetuation of immune-mediated arterial inflammation and cholesterol-induced atherosclerosis. Mice expressing the bacterial transgene ␤-galactosidase exclusively in cardiomyocytes and in smooth muscle cells in lung arteries and the aorta (SM-LacZ), and hypercholesterolemic apolipoprotein E-deficient SM-LacZ mice (SM-LacZ͞apoE ؊/؊ ) developed myocarditis and arteritis after immunization with dendritic cells presenting a ␤-galactosidase-derived immunogenic peptide. Hypercholesterolemia amplified acute arteritis and perpetuated chronic arterial inflammation in SM-LacZ͞apoE ؊/؊ mice, but had no major impact on acute myocarditis or the subsequent development of dilated cardiomyopathy. Conversely, arteritis significantly accelerated cholesterol-induced atherosclerosis. Taken together, these data demonstrate that the linkage of immune-mediated arteritis and hypercholesterolemia favors initiation and maintenance of atherosclerotic lesion formation. Therapeutic strategies to prevent or disrupt such self-perpetuating vicious circles may be crucial for the successful treatment of atherosclerosis.

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Chlamydia Pneumoniae , Cytomegalovirus, and Herpes Simplex Virus in Atherosclerosis of the Carotid Artery

Cited by 295 publications

References 25 publications

Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

Infection-induced inflammatory response of adipocytes in vitro

Linking immune-mediated arterial inflammation and cholesterol-induced atherosclerosis in a transgenic mouse model

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