CHSU Discovery

Abstract
Psoriasis and atherosclerosis are chronic inflammatory conditions linked
by overlapping immunological pathways. Psoriasis, an autoimmune
skin disorder characterized by keratinocyte hyperproliferation and
plaque formation, is associated with an increased risk of cardiovascular
diseases, including atherosclerosis. Epidemiologic studies demonstrate
that this increased risk persists even after adjustment for traditional
cardiometabolic risk factors, highlighting psoriasis as an independent
contributor to cardiovascular disease. Atherosclerosis, a vascular disease
marked by lipid accumulation and immune cell infiltration, can lead to
severe cardiovascular events such as myocardial infarction and stroke.
The immune mechanisms driving both conditions overlap, with psoriasis
contributing to endothelial dysfunction and atherogenesis through the
activation of Th1 and Th17 cells, which produce proinflammatory cytokines
that exacerbate vascular inflammation. Key shared mediators include
tumor necrosis factor-α (TNF-α), interleukin-17A (IL-17A), interleukin-23
(IL-23), and interferon-γ (IFN-γ), which promote macrophage activation,
foam cell formation, and plaque progression.
In this review, we examine the contributions of the bacteria Chlamydia
pneumoniae, Helicobacter pylori, and Porphyromonas gingivalis to the
formation of atherosclerotic plaques by promoting chronic inflammation.
These pathogens induce endothelial dysfunction, oxidative stress, and
cytokine release through innate immune signaling pathways that overlap
with those activated in psoriasis. We also explore the shared immunological
and molecular pathways of psoriasis and atherosclerosis and the potential
role of psoriasis treatments in mitigating the progression of atherosclerosis
by targeting these specific bacteria. Specifically, biologic therapies
targeting TNF-α and IL-17A, commonly used in the management of
psoriasis, may also offer therapeutic benefits in reducing atherosclerotic
risk by modulating bacteria-induced vascular inflammation, supporting
further investigation into their cardiovascular effects.