Lymphocyte responses to Chlamydia antigens in patients with coronary heart disease

Halme, S.; Syrjälä, Hannu; Bloigu, Aini; Saikku, Pekka; Leinonen, Maija; Airaksinen, Juhani; Surcel, Heljä‐Marja

doi:10.1093/oxfordjournals.eurheartj.a015403

Cited by 46 publications

(20 citation statements)

References 21 publications

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“…16 17 40 Therefore, the serological evidence that chronic rather than past C pneumoniae infection is associated with atherosclerosis is not compelling. In fact, the number of cases in studies which found a positive association with both immunoglobulins [19][20][21][22][23][24][25] is similar to that in studies which found no association with either, 16-18 20 26 27 although controls were numerically far greater in the former group (642 and 3069 v 767 and 1382). People with chronic debilitating diseases including heart failure are predisposed to respiratory tract infections and this may be one reason why people with coronary artery disease are more likely to have experienced C pneumoniae infection.…”

Section: Data Sources and Data Extractionsupporting

confidence: 56%

Chlamydia pneumoniae and atherosclerosis

Wong¹,

Ward²

1999

Journal of Clinical Pathology

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Objective-To review the literature for evidence that chronic infection with Chlamydia pneumoniae is associated with atherosclerosis and acute coronary syndromes. Data sources-MEDLINE and Institute of Science and Information bibliographic databases were searched at the end of September 1998. Indexing terms used were chlamydi*, heart, coronary, and atherosclerosis. Serological and pathological studies published as papers in any language since 1988 or abstracts since 1997 were selected. Data extraction-It was assumed that chronic C pneumoniae infection is characterised by the presence of both specific IgG and IgA, and serological studies were examined for associations that fulfilled these criteria. Pathological studies were also reviewed for evidence that the presence of C pneumoniae in diseased vessels is associated with the severity and extent of atherosclerosis. Data synthesis-The majority of serological studies have shown an association between C pneumoniae and atherosclerosis. However, the number of cases in studies that have reported a positive association when using strict criteria for chronic infection is similar to the number of cases in studies which found no association. Nevertheless, the organism is widely found in atherosclerotic vessels, although it may not be at all diseased sites and is not confined to the most severe lesions. Rabbit models and preliminary antibiotic trials suggest that the organism might exacerbate atherosclerosis. Conclusion-More evidence is required before C pneumoniae can be accepted as playing a role in atherosclerosis. Although use of antibiotics in routine practice is not justified, large scale trials in progress will help to elucidate the role of C pneumoniae. (Heart 1999;81:232-238) The organism now known as Chlamydia pneumoniae was first isolated in 1965 in Taiwan. It was subsequently recognised to be a cause of acute respiratory disease 1 giving rise to the acronym TWAR (Taiwan acute respiratory) agent. Chlamydia are unique, obligate, intracellular bacterial pathogens of eukaryotic cells. As they are diYcult organisms to culture, much knowledge about C pneumoniae infections has come from serological studies, many of which, since 1988, have shown an association between C pneumoniae infection and atherosclerosis. However, association does not prove causality and, unfortunately, serological distinction between past and current infection is diYcult.In a general population, infection was absent in children under 5 years, attaining a peak incidence of 9.2% in those aged 5-10 years before falling to 1.5% over the age of 20.2 By the age of 20 years, prevalence of specific IgG has already reached 50%, persisting or even increasing with age.3-5 Seroprevalence is proportional to the product of annual incidence and the duration of seropositivity following infection. As specific IgG antibodies are thought to disappear about three years following primary C pneumoniae infection, 6 an annual incidence of 1.5% should result in a prevalence of 4.5% rather than the observed 50%. ...

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Section: Data Sources and Data Extractionsupporting

confidence: 56%

Chlamydia pneumoniae and atherosclerosis

Wong¹,

Ward²

1999

Journal of Clinical Pathology

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“…In primary infection in healthy people, circulating lymphocytes respond equally to Chlamydia pneumoniae and Chlamydia trachomatis antigens, suggesting that conservative chlamydial structures dominate over the species-specific ones as targets for the cellmediated responses (Halme et al, 1997). The immune escape of chlamydiae within the host includes mechanisms for evasion of T cell recognition by interfering with the expression of MHC molecules.…”

Section: Natividad Et Al (2009) Tried To Investigate How Genetic Varmentioning

confidence: 99%

Host Immune Response to Chlamydia Infection

Carmen¹,

Socolov²,

Veaceslav³

et al. 2012

Chlamydia

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“…14 -20 C pneumoniae has been identified as an antigen that can activate T cells cultured from the peripheral blood of patients with atherosclerotic disease in addition to T cells cultured from carotid atherosclerotic plaque. 9,11,21 In addition, C pneumoniae has been reported to stimulate a cell-mediated immune (CMI) response 9,11,22 that could potentially activate both the CD4ϩ and CD8ϩ T cells through antigenic peptide binding to HLA class II and class I molecules, respectively. [23][24][25] The predominant T-cell type that has been reported from examination of cultured cells from plaques are CD4ϩ T cells, 24 though CD8ϩ T lymphocytes also have been reported.…”

Section: See Editorial Comment Page 1972mentioning

confidence: 99%

Increased CD8 ⁺ T Cells Associated With Chlamydia pneumoniae in Symptomatic Carotid Plaque

Nadareishvili

Koziol

Szekely

et al. 2001

Stroke

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Background and Purpose-The presence of Chlamydia pneumoniae has been reported in carotid atheroma, but its causative effect in the activation of an atherosclerotic plaque to a prothrombotic state remains unproved. Antigenmediated activation of T lymphocytes within plaque may represent a mechanism by which infection can result in plaque conversion. The goal of the present study was to characterize the T-cell subtype profile related to the presence of C pneumoniae in patients with symptomatic versus asymptomatic carotid atherosclerosis. Methods-We studied 14 plaques (5 symptomatic and 9 asymptomatic) positive for C pneumoniae confirmed by polymerase chain reaction and 14 plaques (6 symptomatic and 8 asymptomatic) from age-and stenosis-matched patients negative for C pneumoniae by polymerase chain reaction. T-cell subpopulations of T-helper, T-cytotoxic, and T-memory lymphocytes were identified through indirect enzyme immunohistochemistry with anti-CD3ϩ, anti-CD4ϩ, anti-CD8ϩ, and anti-CD45ROϩ monoclonal antibodies, respectively. Results are expressed as the number of positive cells per millimeter squared. Results-In the absence of C pneumoniae, symptomatic plaques had a modest but significant increase of CD3ϩ (89.

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Lymphocyte responses to Chlamydia antigens in patients with coronary heart disease

Cited by 46 publications

References 21 publications

Chlamydia pneumoniae and atherosclerosis

Chlamydia pneumoniae and atherosclerosis

Host Immune Response to Chlamydia Infection

Increased CD8 ⁺ T Cells Associated With Chlamydia pneumoniae in Symptomatic Carotid Plaque

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Lymphocyte responses to Chlamydia antigens in patients with coronary heart disease

Cited by 46 publications

References 21 publications

Chlamydia pneumoniae and atherosclerosis

Chlamydia pneumoniae and atherosclerosis

Host Immune Response to Chlamydia Infection

Increased CD8 + T Cells Associated With Chlamydia pneumoniae in Symptomatic Carotid Plaque

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Increased CD8 ⁺ T Cells Associated With Chlamydia pneumoniae in Symptomatic Carotid Plaque