Common inflammatory mediators orchestrate pathophysiological processes in rheumatoid arthritis and atherosclerosis

Montecucco, Fabrizio; Mach, François

doi:10.1093/rheumatology/ken395

Cited by 182 publications

(124 citation statements)

References 280 publications

(266 reference statements)

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“…There are several similarities between the inflammatory and immune mechanisms of the atherosclerotic process, the major substrate of CVD and CID (2). Hence, it has been suggested that CID may be associated with a high risk for development of atherosclerosis early in the course of the disease, leading to increased incidence of CVD in the long term (3).…”

Section: Introductionmentioning

confidence: 99%

Changes in vascular function and structure in juvenile idiopathic arthritis

Vlahos¹,

Theocharis²,

Bechlioulis³

et al. 2011

Arthritis Care & Research

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Objective. Chronic inflammatory diseases in adults have been associated with increased cardiovascular risk and impaired vascular function. We aimed to assess the presence of early vascular dysfunction in patients with juvenile idiopathic arthritis (JIA) and investigate the role of inherent inflammatory process of JIA in vascular health. Methods. Thirty patients with JIA (age range 7-18 years) were compared to 33 age-and sex-matched controls. Endothelial function (brachial artery flow-mediated dilation [FMD]), carotid intima-media thickness (IMT), and arterial stiffness were examined. Endothelial inflammation was assessed by intercellular adhesion molecule 1 (ICAM-1) and P-selectin measurements. Results. Patients with JIA showed decreased FMD compared to controls (P ‫؍‬ 0.001), independent of age (P ‫؍‬ 0.9 among age subgroups). Baseline differences in erythrocyte sedimentation rate, ICAM-1, and glucose between the 2 groups accounted for the difference in FMD. The presence of systemic JIA was associated with greater IMT compared to patients with oligoarticular disease, polyarticular disease, or controls (P ‫؍‬ 0.014, P ‫؍‬ 0.069, and P ‫؍‬ 0.046, respectively). The difference in IMT between systemic versus oligoarticular/polyarticular JIA was attributed to the following risk factors: age, body mass index, blood pressure, disease activity, and corticosteroids use. There were no differences in arterial stiffness indices between JIA patients and controls or between patients with systemic versus nonsystemic disease. Conclusion. Endothelial function is impaired in patients with JIA at a very young age, while IMT is increased only in the presence of systemic JIA. Vascular dysfunction may be partly attributed to the effects of disease-related characteristics (inflammation, disease activity, and medications).

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Section: Introductionmentioning

confidence: 99%

Changes in vascular function and structure in juvenile idiopathic arthritis

Vlahos¹,

Theocharis²,

Bechlioulis³

et al. 2011

Arthritis Care & Research

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“…Over the past decade, it has become evident that upregulation of inflammation and autoimmune aggression in certain systemic disorders such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) may substantially accelerate atherogenesis and increase the risk of vascular events [10][11][12]. Basic and clinical research studies in this *Address correspondence to this author at the Boğaziçi University, Department of Molecular Biology and Genetics, 34342 Bebek/Istanbul, Turkey; Tel: +90(212) 359-77-84; Fax: +90 (212) 287-2468; E-mail: sahru.yuksel@boun.edu.tr field have led to the emergence of a new biomedical discipline, vascular rheumatology [13], which aims to clarify pathophysiology of rheumatic diseases and co-morbidities and to propose recommendations for primary and secondary prevention of vascular events in the general population.…”

Section: Introductionmentioning

confidence: 99%

Familial Mediterranean Fever as an Emerging Clinical Model of Atherogenesis Associated with Low-Grade Inflammation

Yüksel¹,

Ayvazyan²,

Gasparyan³

2010

TOCMJ

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Numerous inflammatory and innate immune pathways are involved in atherogenesis. Elaboration of clinical models of inflammation-induced atherogenesis may further advance our knowledge of multiple inflammatory pathways implicated in atherogenesis and provide a useful tool for cardiovascular prevention. Familial Mediterranean fever (FMF) is a chronic inflammatory disorder with profiles of inflammatory markers close to that seen in the general population. In a few recent studies, it has been shown that endothelial dysfunction, increased atherosclerotic burden and activation of platelets accompany attack-free periods of FMF. Colchicine is proved to be useful in suppression of inflammation in FMF. Preliminary basic and clinical studies suggest that this relatively safe drug may be useful for cardiovascular protection in patients with FMF and in the general population. Multinational prospective studies are warranted to further elaborate clinical model of inflammation-induced atherosclerosis associated with FMF.

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“…It has been reported that in patients with various infectious and non-infectious diseases, the production of inflammatory cytokine increases [18]. Also, this condition occurs in other chronic situations such as cystic fibrosis [19], Rheumatoid arthritis and atherosclerosis [18], pulmonary fibrosis, chronic osteomyelitis, and allergic asthma [11] [20] [21] [22]. IL-1 plays an important role in pathogenesis and maintenance of CNS diseases, such as multiple sclerosis, Alzheimer and clinical evolution of coronary artery diseases.…”

Section: Discussionmentioning

confidence: 99%

Measuring Tumor Necrosis Factor-Alpha and Interleukin-1 Beta Levels in Mustard Gas Exposed Patients

Sheibani¹,

Goudarzi²,

Esfandiari³

et al. 2017

ABB

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Sulfur mustard (SM) is an alkalizing chemical which has been used mostly as a weapon all over the world. Sulfur mustard can cause damages to many organs, especially the skin, respiratory system and the eyes. Generally, many complications of mustard gas result from its alkalizing potency and reaction with cellular components like DNA, RNA, proteins and lipid membranes. The damages caused by SM will lead to many complications which persist during the lifespan of exposed subjects. Pro-inflammatory cytokines including especially TNF-α and IL-1β can cause systemic inflammatory reactions and vast changes like altered cell signaling, migration, cytokine production changes and fever. This study was designed to analyze cytokine levels in mustardgas-exposed people's serum in the war between Iraq and Iran, who had the chronic dry-eye symptoms compared to the normal group, 30 years after exposure. In this study, 25 veterans who were exposed to mustard gas were compared to 25 healthy people as control group. The veterans with concurrent involvement of eye, lung, and skin were selected. We used ELISA method to assess the levels of TNF-α and IL-1β in serum of people in both groups. All the results analyzed with T-test in SPSS 17 statistical software. The mean levels of TNF-α and IL-1β in serum of chemical exposed veterans were 52.3 ± 1.4 pg/ml and 3.43 ± 0.3 pg/ml while in the control group were 19.5±1.3 pg/ml and 2.25 ± 0.2 pg/ml, respectively. In the control group, the serum pro-inflammatory cytokine levels were significantly lower than the exposed group (P < 0.05). This study showed that there is a meaningful difference be-

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Common inflammatory mediators orchestrate pathophysiological processes in rheumatoid arthritis and atherosclerosis

Cited by 182 publications

References 280 publications

Changes in vascular function and structure in juvenile idiopathic arthritis

Changes in vascular function and structure in juvenile idiopathic arthritis

Familial Mediterranean Fever as an Emerging Clinical Model of Atherogenesis Associated with Low-Grade Inflammation

Measuring Tumor Necrosis Factor-Alpha and Interleukin-1 Beta Levels in Mustard Gas Exposed Patients

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