Lack of association between Chlamydia Pneumoniae serology and endothelial dysfunction of coronary arteries

Ferrari, Markus; Werner, Gerald S.; Richartz, Barbara M.; Oehme, A.; Straube, Eberhard; Figulla, Hans R.

doi:10.1186/1476-7120-3-12

Cited by 5 publications

(4 citation statements)

References 38 publications

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“…Previous studies have focused on infections with Chlamydia pneumoniae, Cytomegalovirus, herpes simplex virus, Helicobacter pylori, and periodontitis in this context [13,14]. In contrast to these, various other studies have challenged the causal role of infectious agents in atherogenesis [15,16]. What current evidence does suggest, however, is that atherosclerosis may indeed develop in response to inflammatory stimuli.…”

Section: Discussioncontrasting

confidence: 42%

Could there be an association between chronic brucellosis and endothelial damage?

Togan

Çiftçi

Turan

et al. 2015

J Infect Dev Ctries

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Introduction: In this study, we examined the effects of Brucella infection on endothelial dysfunction. Flow-mediated dilatation (FMD) measurement is indicator of the endothelial function, and abnormal values indicating endothelial dysfunction are accepted as the first stage of atherosclerosis. Methodology: Twenty-four patients who had been treated for acute brucellosis two years before, and who had had no relapses in the followup, were prospectively included in the study, along with 30 healthy individuals in the control group. Results: While the highly sensitive Creactive protein (hs-CRP) value was 2.42 ± 1.45 in the patient group, it was 1.72 ± 0.61 in the control group (p = 0.025). While the FMD value was 3.50 ± 1.58 in the patient group, it was 5.88 ± 1.88 in the control group (p < 0.001). While the percentage increase in FMD was 9.88 ± 4.92 in the patient group, it was 17.49 ± 6.3 in the control group (p < 0.001). It was observed that FMD value, the percentage increase in FMD, and basal radius were correlated with hs-CRP (r = -0.644, p < 0.001; r = -0.558, p = 0.002; r = 0.444, p = 0.018, respectively). The carotid artery intima media thickness (IMT) value was found to be 0.61 ± 0.17 in the patient group and 0.49 ± 0.12 in the control group (p = 0.004). Conclusions: The abnormal FMD and IMT values observed in brucellosis patients might be an indicator of more frequent arterial dysfunction, increased cardiovascular risk, and atherosclerosis.

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Section: Discussioncontrasting

confidence: 42%

Could there be an association between chronic brucellosis and endothelial damage?

Togan

Çiftçi

Turan

et al. 2015

J Infect Dev Ctries

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“…Salmonella typhus; vascular injury ENDOTHELIAL PROGENITOR CELLS (EPCs) are circulating mononuclear cells that are mobilized from the bone marrow in response to tissue ischemia or vascular perturbation (2,5,25) and have the capacity to home to sites of injury, differentiate into mature endothelial cells (ECs), and participate in vascular repair. Several studies have reported a correlation between cardiovascular risk factors and reduced circulating EPCs (10,11,45) with a lower EPC count being independently predictive of future cardiovascular events (48).…”

mentioning

confidence: 99%

Circulating endothelial progenitor cells are not affected by acute systemic inflammation

Padfield¹,

Tura²,

Haeck³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Vascular injury causes acute systemic inflammation and mobilizes endothelial progenitor cells (EPCs) and endothelial cell (EC) colony-forming units (EC-CFUs). Whether such mobilization occurs as part of a nonspecific acute phase response or is a phenomenon specific to vascular injury remains unclear. We aimed to determine the effect of acute systemic inflammation on EPCs and EC-CFU mobilization in the absence of vascular injury. Salmonella typhus vaccination was used as a model of acute systemic inflammation. In a double-blind randomized crossover study, 12 healthy volunteers received S. typhus vaccination or placebo. Phenotypic EPC populations enumerated by flow cytometry [CD34+VEGF receptor (VEGF)R-2+CD133+, CD14+VEGFR-2+Tie2+, CD45−CD34+, as a surrogate for late outgrowth EPCs, and CD34+CXCR-4+], EC-CFUs, and serum cytokine concentrations (high sensitivity C-reactive protein, IL-6, and stromal-derived factor-1) were quantified during the first 7 days. Vaccination increased circulating leukocyte (9.8 ± 0.6 vs. 5.1 ± 0.2 × 109cells/l, P < 0.0001), serum IL-6 [0.95 (0–1.7) vs. 0 (0–0) ng/l, P = 0.016], and VEGF-A [60 (45–94) vs. 43 (21–64) pg/l, P = 0.006] concentrations at 6 h and serum high sensitivity C-reactive protein at 24 h [2.7 (1.4–3.6) vs. 0.4 (0.2–0.8) mg/l, P = 0.037]. Vaccination caused a 56.7 ± 7.6% increase in CD14+cells at 6 h ( P < 0.001) and a 22.4 ± 6.9% increase in CD34+cells at 7 days ( P = 0.04). EC-CFUs, putative vascular progenitors, and the serum stromal-derived factor-1 concentration were unaffected throughout the study period ( P > 0.05 for all). In conclusion, acute systemic inflammation causes nonspecific mobilization of hematopoietic progenitor cells, although it does not selectively mobilize putative vascular progenitors. We suggest that systemic inflammation is not the primary stimulus for EPC mobilization after acute vascular injury.

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“…Since the 1980, evidence of the presence of C. pneumoniae in aortic valves has been demonstrated, and the bacterium has been assigned an important role in the calcification process (33). However, failure to detect C. pneumoniae is common using methods such as cell culture isolation or nucleic acid detection in cardiovascular tissues, even in populations with a high prevalence of antibodies (24–36). Biopsies of the coronary artery (37), aorta, and atheroma plaque (38) showed the presence of C. pneumoniae antigens by immunohistochemistry, which might be relevant in the pathogenesis of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Association of Chlamydia trachomatis, C. pneumoniae, and IL-6 and IL-8 Gene Alterations With Heart Diseases

et al. 2019

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Atherosclerosis is a progressive disease characterized by chronic inflammation of the arterial walls, associated with genetic and infectious factors. The present study investigated the involvement of Chlamydia trachomatis and Chlamydia pneumoniae infections and immunological markers (C-reactive protein, CRP, TNF-α, IL-6, IL-8, and IL-10) in the process of atherosclerosis. The evaluation included 159 patients for surgical revascularization (CAD) and 71 patients for surgical heart valve disease (HVD) at three hospitals in Belém, Brazil. The control group (CG) comprised 300 healthy individuals. Blood samples collected before surgery were used for antibodies detection (enzyme immunoassay), CRP (immunoturbidimetry) and IL-6 levels (enzyme immunoassay). Tissue fragments (atheroma plaque, heart valve and ascending aorta) were collected during surgery and subjected to qPCR for detection of bacterial DNA. Promoter region polymorphisms of each marker and relative quantification of TNF-α, IL-8, and IL-10 gene expression were performed. Demography and social information were similar to the general population involved with both diseases. Antibody prevalence to C. trachomatis was 30.6, 20.3, and 36.7% (in the CAD, HVD, and CG, respectively) and to C. pneumoniae was 83.6, 84.5, and 80.3% (in the CAD, HVD, and CG, respectively). C. trachomatis cryptic plasmid DNA was detected in 7.4% of the samples. Frequency of IL6−174G>C polymorphism was higher in CAD and HVD than in CG regardless of previous exposure to Chlamydia. Previous C. trachomatis infection showed involvement in HVD and CAD. Significant association between disease and previous C. pneumoniae infection was found only among HVD. GG genotype of IL6−174G>C is apparently a risk factor for heart disease, whereas AT genotype of IL8−251A>T was mainly involved in valvulopathies, including patients with prior exposure to C. pneumoniae.

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Lack of association between Chlamydia Pneumoniae serology and endothelial dysfunction of coronary arteries

Cited by 5 publications

References 38 publications

Could there be an association between chronic brucellosis and endothelial damage?

Could there be an association between chronic brucellosis and endothelial damage?

Circulating endothelial progenitor cells are not affected by acute systemic inflammation

Association of Chlamydia trachomatis, C. pneumoniae, and IL-6 and IL-8 Gene Alterations With Heart Diseases

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