Chlamydia Pneumoniae and Atherosclerosis: From Koch Postulates to Clinical Trials

Liu, Catherine; Waters, David D.

doi:10.1016/j.pcad.2005.01.001

Cited by 26 publications

(19 citation statements)

References 49 publications

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“…In addition to endogenously generated autoantigens, T cell may recognize antigens produced by infectious organisms that reside in plaques. Perhaps the most extensively studied microbe putatively implicated in the pathogenesis of atherosclerosis in Chlamydia pneumoniae (Cpn) 16. T cells specific for CpN Hsp65 have been isolated from human lesions, and CpN HSP65 has been detected in the majority of human lesions analyzed 17,18.…”

Section: Candidate Atherosclerosis-related T Cell Antigensmentioning

confidence: 99%

“…T cells specific for CpN Hsp65 have been isolated from human lesions, and CpN HSP65 has been detected in the majority of human lesions analyzed 17,18. Nonetheless, studies have failed to show that antibiotic therapy reduces atherosclerosis-related clinical events in patients at risk 16,18. Another candidate antigens that has also been implicated in the pathogenesis of atherosclerosis is β-glycoprotein Ib (β-GPI) 19–21, which is expressed by platelets.…”

Section: Candidate Atherosclerosis-related T Cell Antigensmentioning

confidence: 99%

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T-Cell Costimulation and Coinhibition in Atherosclerosis

Gotsman

Sharpe

Lichtman

2008

Circulation Research

122

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Abstract-Evidence from many human and rodent studies has established that T lymphocytes enhance inflammation in atherosclerotic plaques and contribute to lesion progression and remodeling. Recent work also indicates that regulatory T cells are important in limiting proatherogenic T-cell responses. Given the important role of T cells in atherosclerosis, there is a need to fully understand how proatherogenic T cells are activated and regulated. Antigen-dependent activation of naïve T cells, leading to clonal expansion and effector T-cell differentiation, and effector and memory T cells, is enhanced by signals provided by costimulatory molecules expressed by antigen presenting cells, which bind to receptors on the T cells. In addition, T-cell responses to antigen are negatively regulated by coinhibitory molecules expressed by antigen-presenting cells, which bind to receptors on T cells. Two major families of costimulatory molecules include the B7 and the tumor necrosis factor (TNF) families. These molecules bind to receptors on T cells belonging to the CD28 or TNF receptor families, respectively. The best-defined coinhibitors and their receptors belong to the B7 and CD28 families. Recent work has begun to define how these T-cell costimulatory and coinhibitory pathways influence atherosclerosis, largely in mouse models of the disease. Profound effects are attributable to molecules in both the B7/CD28 (B7-1/2, ICOS, and PDL-1/2) and the TNF/TNF receptor (CD40, OX40, and CD137) families. One emerging theme is that both pathogenic effector T-cell responses and regulatory T cells are influenced by overlapping sets of costimulators and coinhibitors. These complexities must be considered as immunotherapeutic approaches for atherosclerotic disease are developed. (Circ Res. 2008;103:1220-1231.)

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Section: Candidate Atherosclerosis-related T Cell Antigensmentioning

confidence: 99%

Section: Candidate Atherosclerosis-related T Cell Antigensmentioning

confidence: 99%

T-Cell Costimulation and Coinhibition in Atherosclerosis

Gotsman

Sharpe

Lichtman

2008

Circulation Research

122

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“…It has been reported that C. pneumoniae infection is associated with some chronic diseases, including atherosclerosis and neuronal diseases (Balin et al 1998;Sriram et al 1999;Stratton and Sriram 2003;Belland et al 2004;Liu and Waters 2005;Kaperonis et al 2006;Stratton and Wheldon 2006). The diverse function of immune cells results in their playing a central role in the development of such chronic inflammatory diseases.…”

Section: Discussionmentioning

confidence: 99%

“…A number of studies indicate that this bacterium may contribute to the pathogenesis of chronic inflammatory diseases, including atherosclerosis, as demonstrated seroepidemiologically and pathologically (Saikku et al 1988;Kuo et al 1993;Jackson et al 1997;Belland et al 2004;Campbell and Kuo 2004;Liu and Waters 2005). However, the pathophysiological role of C. pneumoniae infection in the development of chronic inflammatory diseases is not well understood.…”

Section: Introductionmentioning

confidence: 99%

Chlamydia pneumoniaeinfection suppressesStaphylococcusenterotoxin B-induced proliferation associated with down-expression of CD25 in lymphocytes

et al. 2010

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Chlamydia pneumoniae (Chlamydophila pneumoniae) infects lymphocytes and modulates their immune functions; this is critical in the development of chronic inflammatory diseases associated with this pathogen. Therefore, to clarify this immune modulation due to C. pneumoniae infection, the effect of this infection on the proliferation of human peripheral blood lymphocytes was examined. Lymphocytes were proliferated by stimulation with Staphylococcus aureus enterotoxin B, and the cell number was increased up to 3 times the unstimulated lymphocyte number. Further, induction of CD25 expression was observed in 55.8% of lymphocytes. Infection with C. pneumoniae suppressed the proliferation of almost half the lymphocytes induced by stimulation with S. aureus enterotoxin B, and CD25 induction was inhibited in 64.7% of lymphocytes. Inhibition of CD25 expression was observed in both infected and uninfected lymphocytes in culture. However, the expression of VLA4 was not affected by C. pneumoniae infection. Furthermore, inhibition was observed only by infection with viable C. pneumoniae and not by the heat-killed bacteria. These results suggest that C. pneumoniae affects lymphocyte function by inhibiting proliferation and CD25 expression in response to immunological stimulation, possibly via humoral mediator(s).

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“…In addition, they were able to demonstrate that if low grade inflammatory response as measured by CRP was taken into consideration then the coronary risk was almost doubled [52]. Since then a number of groups have investigated the association between C.pneumoniae seropositivity and coronary risk [53]. In 1997, Danesh et al published a meta-analysis of 18 seroepidemiological studies [54].…”

Section: A) Chlamydia Pneumoniaementioning

confidence: 99%

Infections and Atheromatous Plaque: Current Therapeutic Implications

Charakida¹,

Tousoulis²

2013

Current Pharmaceutical Design

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Infections are the most common inflammatory triggers and acute and chronic infections have been associated with the development and progression of atherosclerotic disease raising interest in the infectious hypothesis of atherosclerosis. Pathogens have been identified in atherosclerotic plaques and large epidemiological studies have documented conflicting associations between serological evidence of infection and cardiovascular events. Influenza A was mostly studied as a trigger for cardiovascular events during winter months, whilst cytomegalovirus, Chlamydia pneumoniae, helicobacter pylori and porphyromonas ginigivalis were the most studied chronic pathogens which had been associated with the development and progression of cardiovascular disease. Infectious agents can contribute to atherosclerosis by having a direct effect on the vascular wall or via indirect effects including inflammatory responses and molecular mimicry. Efforts to prevent infection with vaccination or treat specific infectious agents with antibiotics have provided mostly negative results, thereby challenging the validity of the infectious hypothesis of atherosclerosis.

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Chlamydia Pneumoniae and Atherosclerosis: From Koch Postulates to Clinical Trials

Cited by 26 publications

References 49 publications

T-Cell Costimulation and Coinhibition in Atherosclerosis

T-Cell Costimulation and Coinhibition in Atherosclerosis

Chlamydia pneumoniaeinfection suppressesStaphylococcusenterotoxin B-induced proliferation associated with down-expression of CD25 in lymphocytes

Infections and Atheromatous Plaque: Current Therapeutic Implications

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