The role of cytomegalovirus and interleukin-8 in destabilization of atherosclerotic lesions in humans

2021 ◽  
Vol 21 (1) ◽  
pp. 11-17
Author(s):  
Svetlana V. Maltseva ◽  
Peter V. Pigarevsky ◽  
Natalya G. Davydova ◽  
Vlada A. Snegova

Relevance. Currently, the role of persistent infections in the atherogenesis development mechanism is not fully understood. Therefore, its important to analyze the role of viral infection against the background of the pro-inflammatory cytokines expression in atherosclerotic plaque destabilization. The aim of the work was a comparative immunohistochemical study of cytomegalovirus (CMV) and IL-8 in different types of human atherosclerotic lesions during their destabilization. Materials and methods. The study was carried out on 130 autopsy samples of human aorta. CMV was detected by direct immunofluorescent antibody staining. IL-8 was detected by two-stage streptavidin-biotin antibody staining. Results. It has been shown that active detection of both CMV and IL-8 is characteristic of atherogenesis foci of the arterial intima with the most intense immune-inflammatory changes. The obtained results indicate the synergism of the cellular response to CMV and IL-8 in the vascular wall during the destabilization atherosclerotic lesions process. Conclusion. According to the results of the work, it can be concluded that both the presence of CMV in atherosclerotic lesions and the high production of IL-8 play a significant role in the formation of unstable atherosclerotic plaques in the vascular wall.

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Emanuela Marcantoni ◽  
Luigia Di Francesco ◽  
Melania Dovizio ◽  
Annalisa Bruno ◽  
Paola Patrignani

Cardiovascular risk factors contribute to enhanced oxidative stress which leads to endothelial dysfunction. These events trigger platelet activation and their interaction with leukocytes and endothelial cells, thus contributing to the induction of chronic inflammatory processes at the vascular wall and to the development of atherosclerotic lesions and atherothrombosis. In this scenario, endogenous antioxidant pathways are induced to restrain the development of vascular disease. In the present paper, we will discuss the role of heme oxygenase (HO)-1 which is an enzyme of the heme catabolism and cleaves heme to form biliverdin and carbon monoxide (CO). Biliverdin is reduced enzymatically to the potent antioxidant bilirubin. Recent evidence supports the involvement of HO-1 in the antioxidant and antiinflammatory effect of cyclooxygenase(COX)-2-dependent prostacyclin in the vasculature. Moreover, the role of HO-1 in estrogen vasoprotection is emerging. Finally, possible strategies to develop novel therapeutics against cardiovascular disease by targeting the induction of HO-1 will be discussed.


2021 ◽  
pp. 1-8
Author(s):  
Inna-Margaryta Radomychelski ◽  
Artem Piddubnyi ◽  
Sergey Danilchenko ◽  
Olena Maksymova ◽  
Yuliia Moskalenko ◽  
...  

Ectopic calcification or pathological biomineralization correlates with morbidity and mortality from cardiovascular diseases. Aortas with atherosclerotic lesions and biomineralization were selected for the study. Thirty samples of mineralized abdominal aortas (group M) were examined by histology. Depending on the calcifications size, samples were separated into group M1 (macroscopic calcifications) and M2 (microscopic calcifications). Each group consists of 15 samples. Calcification 2 mm or less were considered as microscopic, >2 mm—macroscopic. Thirty samples of aortic tissue without biomineralization (group C) were used as a control group. Aortic tissue was examined by macroscopic description, histology, histochemistry, immunohistochemistry (IHC), scanning electron microscopy (SEM) with microanalysis, and transmission electron microscopy (TEM). The results of IHC showed the involvement of OPN in the formation and development of pathological biomineralization, but the obvious role of OPN in the differentiation of macro- and microcalcifications of atherosclerotic aorta was not revealed. SEM with X-ray microanalysis confirmed that the biomineral part of the aortic samples of the M1 group consisted mainly of apatites, which correspond to previous studies. The Ca/P ratio was less in the M2 group than in the M1 group. It means that microcalcifications can be formed by more defective (immature) hydroxyapatite.


2019 ◽  
Vol 8 (4) ◽  
pp. 25-31
Author(s):  
A.M. Markin ◽  
◽  
Yu.V. Markina ◽  
V.N. Sukhorukov ◽  
A.M. Khaylov ◽  
...  

2000 ◽  
Vol 38 (12) ◽  
pp. 4408-4411 ◽  
Author(s):  
Bora Farsak ◽  
Aylin Yildirir ◽  
Yakut Akyön ◽  
Ahmet Pinar ◽  
Mehmet Öç ◽  
...  

Chlamydia pneumoniae and Helicobacter pylori can cause persistent infections of the respiratory and gastrointestinal tract, respectively. It has been suggested that persistent infection of arteries with these bacteria can contribute to the development of atherosclerosis. The aims of this study were to determine the presence of C. pneumoniae and H. pylori DNA in atherosclerotic plaque samples by PCR and to evaluate the correlation between clinical status and DNA positivity of these bacteria. Eighty-five consecutive patients (mean age, 59 ± 10; 75 male, 10 female) undergoing coronary artery bypass grafting, carotid endarterectomy, and surgery of the abdominal aorta for atherosclerotic obstructive lesions were included in the study. Forty-six endarterectomy specimens from the atherosclerotic lesions and 39 specimens from healthy regions of the ascending aorta, which were accepted as the control group, were excised. The presence of microorganism DNA in endarterectomy specimens was assessed by PCR.C. pneumoniae DNA was found in 12 (26%) of 46 endarterectomy specimens and none of the healthy vascular-wall specimens (P < 0.001), while H. pyloriDNA was found in 17 (37%) of 46 endarterectomy specimens and none of the controls (P < 0.001). Either C. pneumoniae or H. pylori DNA was positive in 23 (50%) of 46 patients and none of the controls (P < 0.001). Six of the atherosclerotic lesions showed coexistence of both of the microorganism DNAs. The presence of C. pneumoniae andH. pylori DNA in a considerable number of atherosclerotic plaques but their absence in healthy vascular wall supports the idea that they may have a role in the development of atherosclerosis, especially in countries where infection is prevalent and where conventional risk factors fail to explain the high prevalence of atherosclerotic vascular disease.


2019 ◽  
Vol 19 (2) ◽  
pp. 7-12
Author(s):  
Peter V. Pigarevsky ◽  
Olga G. Yakovleva ◽  
Svetlana V. Maltseva ◽  
Veronica A. Guseva

The review examined of the processes of cell proliferation in human vascular wall and experimental animals during the formation of atherosclerotic plaques. Shows the types of actively proliferating cells: lymphocytes, macrophages, endotheliocytes and zones identified in the vascular wall, where this proliferation occurs. The factors that promote and hinder cell proliferation during the growth of atherosclerotic plaque are identified. The survey shows all the stages of the formation of atherosclerotic lesions, ranging from normal plots and lipid stains to pronounced fibrous plaques. Establishes a link between the cell proliferation and inflammation in the vascular wall man. Separately considered the role of cell proliferation in the destabilization of atherosclerotic plaque. If atherosclerosis this process still poorly studied, in the formation of unstable atherosclerotic plaques in humans it is completely unknown. Based on your own original data was finally on the important role of the processes of cell proliferation in the formation of unstable atherosclerotic plaques in humans.


1982 ◽  
Vol 48 (02) ◽  
pp. 201-203 ◽  
Author(s):  
N A Marsh ◽  
P J Gaffney

SummaryThe effect of strenuous exercise on the fibrinolytic and coagulation mechanisms was examined in six healthy male subjects. Five min bicycle exercise at a work-rate of 800 to 1200 kpm. min−1 produced an abrupt increase in plasma plasminogen activator levels which disappeared after 90 min. However, there was no change in early or late fibrin degradation products nor was there a change in fibrinopeptide A levels or βthromboglobulin levels after exercise although activated partial thromboplastin times were significantly shortened. It is concluded that strenuous exercise does not produce any real increase in fibrinogen-fibrin conversion nor any real increase in the breakdown of these proteins. The role of exercise-induced release of plasminogen activator remains unclear, but probably helps to maintain plasma levels in a discontinuous manner concurrently with the continuous low-level secretion from the vascular wall. The shortening of partial thromboplastin time may be due to the raised levels of plasminogen activator changing the activation state of other coagulation factors.


Author(s):  
A. Kulikov

Presented material reveals main links in the pathogenesis of hemostatic disorder. In particular, attention is paid to the role of the lungs, liver and other organs in the development of this process. Role of vascular wall and blood cells in regulation of the physical state of blood is described in detail. The most frequent factors leading to hypercoagulation are indicated. Difference between hypercoagulation and thrombophilia is shown. The latter is found in clinical practice quite often, but at the same time, it is poorly diagnosed. Such a terrible complication of hemostatic disorder as disseminated intravascular coagulation is described. Its classification, stages of development, clinical manifestations are offered to the readers.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Kenji Inoue ◽  
Tatsuhiko Kodama ◽  
Hiroyuki Daida

Numerous studies have recently examined the role of pentraxin 3 (PTX3) in clinical situations. The pentraxin family includes C-reactive protein (CRP); however, unlike CRP, PTX3 is expressed predominantly in atherosclerotic lesions that involve macrophages, neutrophils, dendritic cells, or smooth muscle cells. Interestingly, PTX3 gene expression in human endothelial cells is suppressed to a greater extent by pitavastatin than the expression of 6,000 other human genes that have been examined, suggesting that PTX3 may be a novel biomarker for inflammatory cardiovascular disease. The expression and involvement of PTX3 in cardiovascular diseases are discussed in this paper, along with the characteristics of PTX3 that make it a suitable biomarker; namely, that the physiological concentration is known and it is independent of other risk factors. The results discussed in this paper suggest that further investigations into the potential novel use of PTX3 as a biomarker for inflammatory cardiovascular disease should be undertaken.


Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1184
Author(s):  
Jean-Marc Zingg ◽  
Adelina Vlad ◽  
Roberta Ricciarelli

Levels of oxidized low-density lipoproteins (oxLDLs) are usually low in vivo but can increase whenever the balance between formation and scavenging of free radicals is impaired. Under normal conditions, uptake and degradation represent the physiological cellular response to oxLDL exposure. The uptake of oxLDLs is mediated by cell surface scavenger receptors that may also act as signaling molecules. Under conditions of atherosclerosis, monocytes/macrophages and vascular smooth muscle cells highly exposed to oxLDLs tend to convert to foam cells due to the intracellular accumulation of lipids. Moreover, the atherogenic process is accelerated by the increased expression of the scavenger receptors CD36, SR-BI, LOX-1, and SRA in response to high levels of oxLDL and oxidized lipids. In some respects, the effects of oxLDLs, involving cell proliferation, inflammation, apoptosis, adhesion, migration, senescence, and gene expression, can be seen as an adaptive response to the rise of free radicals in the vascular system. Unlike highly reactive radicals, circulating oxLDLs may signal to cells at more distant sites and possibly trigger a systemic antioxidant defense, thus elevating the role of oxLDLs to that of signaling molecules with physiological relevance.


Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1334
Author(s):  
Ye Liu ◽  
Zahra Mohri ◽  
Wissal Alsheikh ◽  
Umber Cheema

The development of biomimetic, human tissue models is recognized as being an important step for transitioning in vitro research findings to the native in vivo response. Oftentimes, 2D models lack the necessary complexity to truly recapitulate cellular responses. The introduction of physiological features into 3D models informs us of how each component feature alters specific cellular response. We conducted a systematic review of research papers where the focus was the introduction of key biomimetic features into in vitro models of cancer, including 3D culture and hypoxia. We analysed outcomes from these and compiled our findings into distinct groupings to ascertain which biomimetic parameters correlated with specific responses. We found a number of biomimetic features which primed cancer cells to respond in a manner which matched in vivo response.


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