Psoriasis and cardiovascular risk: Immune-mediated crosstalk between metabolic, vascular and autoimmune inflammation

Frers, Rodolfo A. Kölliker; Bisoendial, Radjesh J.; Montoya, Sandra Fabiana; Kerzkerg, E.; Castilla, Rocı́o; Tak, PP; Milei, José; Capani, Francisco

doi:10.1016/j.ijcme.2015.01.005

Cited by 22 publications

(27 citation statements)

References 146 publications

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“…crossroads of the cytokine-induced pathogenesis of dilated cardiomyopathy. The SOCS3 transgene induces Th2 responses, and SOCS3 gene deletion did not enhance Th1 polarization as expected but induced a negative regulator of the Treg subset with increased IL-10 and TGFβ production in mice [39,41]. Not only SOCS3 is essential for G-CSF, IL-6, LIF, and leptin signaling, but is also an indirect regulator of IFNγ signaling and a negative regulator of IL-23 signaling, inducing IL-17-secreting T cells (Th17) polarization ( Table 1).…”

Section: Suppressor Of Cytokine Signaling Proteins Immune Regulationmentioning

confidence: 52%

“…They were, as their name suggests, first described as cytokine signaling inhibitors as observed for the Janus kinase/Signal Transducer and Activator of Transcription/ Suppressor of Cytokine Signaling (JAK/STAT/SOCS) signaling pathway (JSS-SP). The remodeling by cytokine receptor signaling mediated by the JSS-SP provides a morphological basis explaining the pathogenesis of myocardial hypertrophy, fibrosis, and inflammation [41] in CCC. The inflammatory markers TNFα, and IL1-β represent potential targets in cardioprotection and therapy [42].…”

Section: Suppressor Of Cytokine Signaling Proteins Immune Regulationmentioning

confidence: 99%

“…The immune-inflammatory response plays a key role in cardiovascular damage [40,41], and T. cruzi-derived molecules may sustain the TLR-mediated innate immune response inducing inflammatory cytokines and chemokines secretion. The adaptive immune response to Chagas antigens may protect the host from secondary reinfection, though damaging the CV system due to inflammation, and the associated connective repair (fibrosis).…”

Section: Long-lasting Systemic Inflammatory Burden and Clinical Chagamentioning

confidence: 99%

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Chagas Cardiomyopathy: Role of Sustained Host-Parasite Interaction in Systemic Inflammatory Burden

Kölliker-Frers¹,

Otero‐Losada²,

Razzitte³

et al. 2018

Chagas Disease - Basic Investigations and Challenges

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The economic and social burden associated with Chagas disease morbidity and mortality is regrettably large in Latin America causing more deaths than does any other parasitic disease. Inflammatory dilated cardiomyopathy is, by far, the most important clinical consequence of Trypanosoma cruzi infection. The insidious persistence of this parasite determines chronic myocarditis progression. The clinical outcome is multifactorial and depends on the particular parasite strain and virulence factors, the infective load and route of infection, the parasite ability to by-pass the protective immune response, the intensity and type of immune response during the acute infective phase, and the host genetic background. From the immunological viewpoint, host control of T. cruzi has been shown to depend on both humoral and cell-mediated adaptive responses and from the innate immune system. In this review, we discuss the most relevant literature conveying information on the relevance of identifying a subset of systemic inflammatory molecules as potential markers of cardiovascular risk morbidity and mortality in patients with Chagas disease. Concurrently, a direct role for the parasite in the perpetuation of myocardial inflammation is substantiated. Ultimately, host-parasite interactions determine the course of the ongoing systemic inflammation and the perpetuation of myocardial inflammation in genetically predisposed patients.

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Section: Suppressor Of Cytokine Signaling Proteins Immune Regulationmentioning

confidence: 52%

Section: Suppressor Of Cytokine Signaling Proteins Immune Regulationmentioning

confidence: 99%

Section: Long-lasting Systemic Inflammatory Burden and Clinical Chagamentioning

confidence: 99%

See 1 more Smart Citation

Chagas Cardiomyopathy: Role of Sustained Host-Parasite Interaction in Systemic Inflammatory Burden

Kölliker-Frers¹,

Otero‐Losada²,

Razzitte³

et al. 2018

Chagas Disease - Basic Investigations and Challenges

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“…Psoriasis is a chronic immunologically mediated dermatosis, affecting 2-3% of the general population (1)(2)(3). Multiple mechanisms are involved in its pathogenesis, such as the hyper-reactivity of T-lymphocytes and dendritic cells, excessive inflammatory cytokine synthesis, accelerated epidermal turnover, epidermal hyperproliferation, reduced keratinocyte differentiation, overexpression of angiogenesis and oxidative stress (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Correlations between related-purine derivatives and renal disorders in patients with psoriasis vulgaris

et al. 2018

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Recent data suggest that severe psoriasis is an independent risk factor for chronic renal disease. In the present study, we investigated the role of related-purine derivatives as predictors of renal dysfunctions in patients with psoriasis. A prospective study was conducted on a group of 45 patients with psoriasis vulgaris and 45 control cases, monitored over a 5-year period. Alterations of renal function, albumin/creatinine ratio (ACR, mg/g) and UA/creatinine ratio (UACR, mg/mg) were determined in spontaneous urine samples. The status of related-purine derivatives was evaluated by quantification of uric acid (UA, mg/dl), adenosine deaminase (ADA, UI/mg protein), xanthine oxidase (XO, UI/mg protein) and 8-hydroxy-deoxy-guanosine levels (8-OHdG, ng/ml) in serum samples. Compared to the controls, in patients with psoriasis there was an increase in related-purine derivatives levels, which was demonstrated by the elevated serum levels of UA (5.1±0.4 vs. 5.4±1.0, P=0.066), ADA (0.14±0.08 vs. 0.29±0.12, P=0.052), XO (0.22±0.11 vs. 0.42±0.21, P=0.011) and 8-OHdG (3.1±0.05 vs. 8.3±4.7, P=0.002). The serum levels of related-purine derivatives were associated with the severity of psoriasis. In addition, there was a link between the serum levels of related-purine derivatives and markers of renal impairment. There were positive correlations between 8-OHdG and ACR (r=0.452, P=0.028) and between ADA, XO, UA, 8-OHdG and UACR (r=0.297 and P=0.032, r=0.301 and P=0.002, r=0.431 and P=0.027, r=0.508 and P=0.002) and negative correlations between UA, 8-OHdG and the estimated glomerular filtration rate (r=-0.301 and P= 0.036, r=-0.384 and P= 0.002). Thus, severe psoriasis is a risk factor for the development of renal disease.

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“…В то же время у больных ПсА и Пс, кроме воспаления, значительная роль в возникновении кардиоваскулярного риска при-надлежит и накоплению традиционных факторов, таких как АГ, дислипидемия, ожирение, курение, снижение физической активности. Сочетание традиционных фак-торов кардиоваскулярного риска и системного воспале-ния при Пс и ПсА, по-видимому, объясняет высокий уровень распространенности ССЗ и повышенный, по сравнению с популяцией, кардиоваскулярный риск при этих заболеваниях [24,25].…”

Section: результатыunclassified

The Pattern of Cardiovascular Comorbidity in Patients With Severe Forms of Psoriasis: Data of Retrospective Analysis of a Hospital Cohort

Баткаева¹,

Коротаева²,

Баткаев³

2017

rsp

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Psoriasis and cardiovascular risk: Immune-mediated crosstalk between metabolic, vascular and autoimmune inflammation

Cited by 22 publications

References 146 publications

Chagas Cardiomyopathy: Role of Sustained Host-Parasite Interaction in Systemic Inflammatory Burden

Chagas Cardiomyopathy: Role of Sustained Host-Parasite Interaction in Systemic Inflammatory Burden

Correlations between related-purine derivatives and renal disorders in patients with psoriasis vulgaris

The Pattern of Cardiovascular Comorbidity in Patients With Severe Forms of Psoriasis: Data of Retrospective Analysis of a Hospital Cohort

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