Psoriasis as a human model of disease to study inflammatory atherogenesis

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 312; no. 5; pp. H867 - H873
• Main Authors: Harrington, Charlotte L, Dey, Amit K, Yunus, Raza, Joshi, Aditya A, Mehta, Nehal N
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.05.2017
• Series: Inflammation, Immunity, and Cardiovascular Disease
• Subjects: Angiography; Atherosclerosis; Atherosclerosis - diagnostic imaging; Atherosclerosis - pathology; Biomarkers; Cardiovascular disease; Computed tomography; Cytokines; Cytokines - metabolism; Heart diseases; Humans; Inflammation - diagnostic imaging; Inflammation - pathology; Inflammatory diseases; Medical imaging; Methotrexate; Models, Biological; Modulation; Pathogenesis; Positron emission; Positron-Emission Tomography; Psoriasis; Psoriasis - diagnostic imaging; Psoriasis - pathology; Review; Risk assessment; atherosclerosis; cardiovascular imaging; 18fludeoxyglucose-positron emission tomography/computed tomography; inflammation; psoriasis
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00774.2016

Inflammation is known to play a significant role in the process of atherogenesis and cardiovascular disease (CVD). Indeed, patients with chronic inflammatory diseases are at increased risk for cardiovascular events. However, the mechanisms linking chronic inflammation and CVD remain poorly understood. Psoriasis, a chronic inflammatory skin disease associated with a greater risk of early cardiovascular events, provides a suitable human model to study the pathophysiology of inflammatory atherogenesis in humans. Additionally, cytokines such as TNF-α, IL-17A, and other immune pathways are the common links between the pathogenesis of psoriasis and atherosclerosis, and hence the approved treatments for psoriasis, which include selective cytokine inhibition (e.g., anti-TNF, anti-IL-17A, and anti-IL-12/23) and immune modulation (e.g., methotrexate or cyclosporine), provide an opportunity to examine the effect of modulating these pathways on atherogenesis. We have been using this human model in a large, prospective cohort study, and this review summarizes our approach and results of using this human model to study inflammatory atherogenesis. Specifically, we review simultaneous multimodal imaging of several vascular beds using fludeoxyglucose positron emission tomography/computed tomography, fludeoxyglucose positron emission tomography/MRI, and coronary computed tomography angiography as well as cardiovascular biomarkers to better understand how modulation of inflammation may impact vascular diseases.