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Although multiple CVR factors are associated with Ps, key components of the metabolic syndrome are more strongly connected with more severe Cutaneous psoriasis PsC [ 28 ]. Recent studies [ 29 ] suggest an increased inflammatory burden in PsA compared with Ps Table 1. In contrast, the risk of developing a CV event MI, ischemic stroke, and transient ischemic attack was not elevated in early Ps patients in a matched follow-up study, case-control analysis [ 30 , 31 ].

Since a substantial amount of data accumulates in the past of this issue, we provide a brief insight into the most common inflammation-related and non-inflammatory factors involved in accelerated atherogenesis in Ps and PsA. Toll-like receptor 2 TLR-2 and toll-like receptor 4 TLR-4 trigger receptor-mediated events, including cytokine-mediated inflammation, are involved in atherosclerosis [ 44 ], Ps, and other pathologies [ 34 ]. Cytokine-triggered TLRs activation is known to modulate major pathological processes, including inflammation, angiogenesis, tissue remodeling, and fibrosis.

These effects are linked to systemic inflammation and lead to a proatherogenic profile. Indeed, atherogenic lipid alterations, oxidative stress abnormalities, vascular injury repair failure, arterial stiffness, insulin resistance induction, endothelial dysfunction, hypercoagulable state, homocysteine elevation, and pathogenic T cell up-regulation could all be attributed in part to the proinflammatory actions of cytokines.

Some molecules listed before and other PsA-related serum cytokine patterns have been demonstrated by multiplex cytokine array systems in Norwegian PsA patients [ 50 , 51 ]. Few of these cytokines previously mentioned [ 52 , 53 ] and their pathogenic contribution at different stages in the pathobiology of atherothrombosis and PsA are not clear yet [ 36 ].

NK cells increase the susceptibility to PsA [ 51 ] and the inflammatory infiltrate in psoriatic skin lesions. Although more studies must be done, emerging evidence supports a role for NK cells in Ps. Therefore, adipose immune cell phenotype and function may provide greater insight into cardio-metabolic pathophysiology in psoriasis [ 54 , 55 ]. NKT cells are a heterogeneous subset of T cell lineage lymphocytes that bear NK cell molecules and T cell receptors, which recognize microbial glycolipids and their own endogenous mammalian lipids presented by the MHC I-like molecule CD1d and have been implicated in the pathogenesis of various autoimmune diseases including Ps.

Due to the numerous functions of NKT cells that link innate and adaptive immunity, their role in Ps is complex and still elusive. Our knowledge of biologically active serum molecules and cells involved in the pathogenesis of both PsA and atherosclerosis is still not clear enough.

Taken together, cytokines seem to play a pivotal role as the major link between PsA and atherosclerosis. Compiled data show that untreated PsA inflammation could produce damage to the CV system even before it affects the joints [ 50 ]. Current evidence suggests that the pathway of inflammation in atherosclerosis culminates in altered concentrations of various markers in peripheral blood, including oxidative stress molecules [ 58 — 60 ] and markers of vascular inflammation like CRP [ 59 ], IL-6, ICAM-1, and MCP-1 [ 61 ].

The majority of epidermal CTL and Th1 effector lymphocyte populations and molecules are elevated in Ps vulgaris lesions and in circulating blood in psoriatic patients [ 64 ]. As an inflammatory cytokine, IL-6 regulates chemokine-directed leukocyte trafficking and directs transition from innate to adaptive immunity through the regulation of leukocyte activation, differentiation, and proliferation [ 68 ]. IL-6 and their signaling events contribute to hepatic release of acute-phase reactants including CRP levels, atherosclerotic plaque development and destabilization [ 69 , 70 ]. IL-6 may also contribute to atherosclerosis and arterial thrombosis by activating the production of tissue factor, fibrinogen and factor VIII; increasing endothelial cell adhesiveness and stimulating platelet production and aggregation [ 71 ].

IL-6 decreases cardiac contractility via a nitric oxide NO -dependent pathway activating STAT3-dependent anti-inflammatory signal transduction [ 78 ]. Numerous studies show a strong association between IL-6 and joint immune-mediated diseases. Mice deficient in mast cells are comparatively resistant in experimentally induced arthritis.

In addition, it is a major promoter of bone resorption in pathological conditions [ 79 ]. In particular, IL-6 has a pivotal role in synovitis, bone erosion, and in the systemic features of inflammation [ 80 ]. In Ps, most available evidence indicates that the pathogenic action of IL-6 is important. The family of endothelins ET includes three aminoacid isoforms endothelin-1 ET-1 , endothelin-2 ET-2 , and endothelin-3 ET-3 , which have endogenous pressor activity and are secreted by different tissues and cells.

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In addition, ET-1 is a vasoactive peptide that induces vasoconstriction, inflammation, and fibrosis and has mitogenic potential for SMC [ 84 ]. In the skin, ET-1 participates in keratinocyte proliferation, neoangiogenesis, and chemotaxis. Its levels are elevated in psoriatic lesions and serum of patients with Ps [ 85 ]. Synovial tissue and serum of patients with PsA all show strongly enhanced ET-1 receptor expression [ 86 ].


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A considerable amount of evidence implicates C-reactive protein CRP as a predictive marker for future CV events and mortality in different settings, particularly under metabolic syndrome conditions in the general population [ 87 , 88 ]; CRP has also been implicated as a direct partaker [ 7 , 89 , 90 ]. In vitro, studies provide evidence for direct proatherogenic effects of CRP, including increased endothelial dysfunction [ 92 ].

Adipose tissue influences both natural and adaptive immunities and links inflammation, metabolic dysfunction, and cardiovascular disease [ 94 ]. MMP-1 serum levels and gene expression are elevated in PsA [ 96 ]. Specifically, both are associated with Th1 and CTL cytotoxic T lymphocyte effector cell-mediated events in vivo [ 68 ], and are elevated in circulating blood [ 63 ].

In contrast, the T-regulatory activity is reduced. Myeloid dendritic cells can stimulate both memory and naive T cells, and are the most potent of all the antigen-presenting cells in normal and various pathophysiological conditions [ 97 ]. In turn, activated T cells undergo firm adhesion and transendothelial migration to inflammatory focus. Extravasation is orchestrated by the combined action of cellular adhesion receptors and chemotactic factors in a wide variety of cardiovascular and autoimmune disorders that involve inflammation.

The development and maintenance of psoriatic plaque are dependent on the participation of infiltrating T lymphocytes CD4 and CD8 and local antigen-presenting cells APCs Langerhans cells, myeloid, and plasmacytoid-DC. IL stimulates the secretion of IL by Th17 cells, which may be involved in epidermal hyperplasia [ 5 ]. The effects of ILA-producing T-helper 17 Th17 cells include suppressive effects of T-regulatory Treg subsets, which have also been implicated in both pathologies. The association of ILA with Ps and PsA has been extensively described [ 98 , 99 ] and a growing body of evidence suggests that ILA might also be involved in atherosclerosis [ ].

IL seems to have a modulatory role in atherosclerosis, but studies available show contrasting results, which could be attributed to different approaches and models.

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Coronary syndrome correlates with increased IL levels [ ]. Ps and coronary artery disease patients show impaired inhibitory function of Treg [ , ]. Humoral response seems to protect rather than harm the host. Several lines of evidence support the hypothesis that humoral immunity protects patients against atherosclerosis. First, the injection of immunoglobulin preparations inhibits atherosclerosis. Second, spleen removal a B-cell rich lymphoid organ seems to deteriorate vascular disease condition.

Third, oxidized LDL plus adjuvant immunization promote atheroprotection [ 2 ]. Evidence so far indicates that atheroprotection is due to a T cell dependent B-cell-mediated mechanism, probably involving antibody dependent clearance of LDL and humoral dependent regulation of pathogenic T cell [ 17 ]. This atheroprotective response must be confirmed in humans. Additionally, certain human leucocyte antigen HLAs are more common in psoriatic arthritis.

PCSK9 inhibitors could ameliorate cardiovascular disease by immune mechanisms

Some molecules of the innate immune system have an important influence on the pathophysiology of psoriasis, such as TLR2 and TLR4 play a key role in the pathogenesis of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjogren's syndrome, psoriasis, multiple sclerosis, and autoimmune diabetes [ ]. Additionally, the expression of TLR2 and TLR4 correlates with the degree and severity of coronary disease [ , ] oxidized phospholipids stimulate the TLR signaling pathway to induce inflammatory cytokine secretion by macrophages and endothelial cells [ ].

Anti-CD14 and anti-TLR antibodies significantly inhibit the binding of fluorescein-labeled LDL to monocytes and interfering with cytokine release [ ].


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These genes strengthened the assertion that psoriasis is an immune disorder, as these genes are linked to both the innate and adaptive immune response [ — ]. In summary, defects in these genes could amplify an inflammatory response by interfering with normal negative feedback of the NF-kB signal and therefore would link to psoriasis with other IMID and coronary pathology. Ps, PsA, and atherosclerosis share disturbances in different metabolic pathways involving insulin-dependent diabetes mellitus IDDM , dyslipidemia, hypertension, obesity, and mostly metabolic syndrome, which may be related to an increase in the prevalence of CVD to their capability of inducing inflammation on the endothelial lining to initiate the process of atherosclerosis.

So far, no pathophysiological mechanism for this association has been identified [ 63 ]. Several studies have found an increase in the prevalence of hypertension in Ps patients, although the definition of hypertension is very heterogeneous among these studies [ — , ]. Other authors have not observed a significant association between Ps and hypertension [ ].

IDDM is responsible for metabolic alterations, accompanied by chronic inflammation and endothelium dysfunction. Observational studies show that the risk of IDDM is higher in patients with Ps compared with a healthy control group. This risk increases with the duration and severity of Ps and it is not related to a high body mass index BMI alone [ ]. In a case-control study from Israel, the risk of diabetes was significantly higher in individuals with Ps [ ]. Recent studies have shown that obesity may precede the onset of Ps as a risk factor [ ], whereas a higher BMI is associated with more severe skin disease activity [ 3 ].

The influence of obesity on psoriatic diseases is the result of complex interactions of inflammatory and metabolic factors. The proinflammatory cytokines stimulate adipocytes to synthesize neuropeptides and more cytokines, which are critical in the pathogenesis of the psoriatic and CVD [ 69 ]. Heavy and long-term smoking [ ] have been associated with increased Ps risk in both men and women [ ], particularly pustular Ps [ , , ]. Smoking increases oxidative damage, promotes inflammatory changes, and enhances Ps-associated gene expression [ ] and CVR [ 50 , ]. Ps patients have a higher prevalence of dyslipidemia and triglycerides and lower prevalence of HDL levels.

Role of innate and adaptive immune mechanisms in cardiac injury and repair.

However, associations with total cholesterol and LDL have not been found statistically significant in a multivariate analysis study [ — ]. The metabolic syndrome is characterized by increases in the immunological activity of Th1, which suggests it may be associated with Ps because of shared inflammatory pathways. Gisondi et al. Recently, Raychaudhuri et al.

Ps with metabolic syndrome [ ] associates with high serum uric acid levels that correlate with an increased risk of carotid intima-media thickness IMT or with the presence of carotid plaques [ ]. Anti-inflammatory effect of 3-Bromo-4,5-dihydroxybenzaldehyde, a component of polysiphonia morrowii , in vivo and in vitro.

Toxicol Res. Treatment with 3-bromo-4, 5-dihydroxybenzaldehyde improves cardiac function by inhibit macrophage infiltration in mice. Frangogiannis NG. The inflammatory response in myocardial injury, repair, and remodelling. Nat Rev Cardiol. Meta-analysis of corticosteroid treatment in acute myocardial infarction. Am J Cardiol. Huang S, Frangogiannis NG. Anti-inflammatory therapies in myocardial infarction: failures, hopes and challenges.


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    Immunity, atherosclerosis and cardiovascular disease | BMC Medicine | Full Text

    Clin Hypertens. Support Center Support Center. Targeting risk factors for atherosclerosis has reduced the death rate, but new therapies are needed to stabilise atherosclerotic plaques and to treat heart blood vessel inflammation to reduce the risk of recurrent heart attacks. Screen music and the question of originality - Miguel Mera — London, Islington. Edition: Available editions United Kingdom. Rahul Kurup , Heart Research Institute. How does the immune system affect the heart? Further Reading: How Australians Die: cause 1 — heart diseases and stroke So this means we now have a marker to tell us who will be at higher risk of heart attack and stroke, even if they have healthy lifestyles.

    Treatment Heart attack victims are particularly vulnerable in the period just after their attack, because the inflammation in the arteries can lead to more plaque becoming unstable and chipping off. Heart disease Immune system Heart attack Inflammation. Pourquoi si sain? Computers may play an important role in preparing us for the next viral outbreak — whether flu or Ebola. UW Institute for Protein Design.

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