Potential Immunological Links Between Psoriasis and Cardiovascular Disease

Abstract

Preclinical and clinical research provide strong evidence that chronic, systemic inflammation plays a key role in development and progression of atherosclerosis. Indeed, chronic inflammatory diseases, such as psoriasis, are associated with accelerated atherosclerosis and increased risk of cardiovascular events. Contemporary research has demonstrated plausible mechanistic links between immune cell dysfunction and cardiometabolic disease in psoriasis. In this review, we describe the role of potential common immunological mechanisms underlying both psoriasis and atherogenesis. We primarily discuss innate and adaptive immune cell subsets and their contributions to psoriatic disease and cardiovascular morbidity. Emerging efforts should focus on understanding the interplay among immune cells, adipose tissue, and various biomarkers of immune dysfunction to provide direction for future targeted therapy.

A Phase IV, Randomized, Double-Blind, Placebo-Controlled Crossover Study of the Effects of Ustekinumab on Vascular Inflammation in Psoriasis (the VIP-U Trial)

“…These findings combined suggest that the improvement in AVI after 12 weeks of ustekinumab is transient. We also evaluated the effect of ustekinumab on key markers of inflammation, lipid, and glucose metabolism, most known to be dysregulated in patients with psoriasis, associated with adverse atherosclerotic outcomes and/or incident diabetes mellitus (Sajja et al, 2018). After 12 weeks of therapy, those treated with ustekinumab had an increase in LDL (20 mg/dl on average) and LDL particle number (200 on average), but these changes were transient and were not sustained at 52 weeks.…”

“…The biologic mechanisms linking psoriasis to adverse cardiometabolic outcomes are multifactorial and complex, given multiple pathways involved in atherosclerotic diseaserelated cardiovascular events (Sajja et al, 2018). These phenotypically distinct clinical states share many immune (e.g., increases in IL-1, IL-6, tumor necrosis factor [TNF], Creactive protein) and metabolic (dyslipidemias and insulin resistance) abnormalities (Azfar and Gelfand, 2008;Mehta et al, 2012a;Sajja et al, 2018). Indeed, IL-1 and IL-6 have been causally linked to cardiovascular disease through clinical trials and Mendelian randomization studies, respectively (Consortium, 2012, Ridker et al, 2017.…”

Psoriasis and Cardiovascular Disease: A Narrative Review

“…Neutrophils also play a role in atherosclerosis and independently predict endothelial dysfunction, linking psoriasis and CV diseases. 22) Some risk factors are shared between psoriasis and CV risk and can exacerbate inflammation in diseases such as those for diabetes, hypertension, smoking, obesity, and dyslipidemia. 3,23) Inflammation is a prime factor in the development of atherosclerotic plaques and increases the risk of rupture resulting in the formation of a thrombus.…”

The Risk of Systemic Diseases in Those with Psoriasis and Psoriatic Arthritis: From Mechanisms to Clinic

“…Pathophysiological mechanisms involved in the association of CVD with psoriasis and PsA can be explained by multifactorial etiologies including genetics, T helper (Th)1- and Th17-pathways, neutrophils, angiogenesis, and dysfunctions of endothelial cells and adipose tissues [ 43 , 44 , 45 , 46 ].…”

“…Psoriasis has long been known as a T-cell mediated inflammatory disease. Th1 polarization of the immune system is associated with the induction of psoriatic inflammation by activating various cells including neutrophils, macrophages, and T lymphocytes to release cytokines such as interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and IL-2 [ 46 ]. These Th1 cytokines are also crucial in the formation and progression of atherosclerotic plaque which is important in the pathogenesis of atherosclerosis [ 51 ].…”