Shared Inflammatory Pathways in Psoriasis and Atherosclerosis: Bacterial Contributions and Therapeutic Implications

Author(s): Felicia Hung and Reena Lamichhane-Khadka

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.