The expression of interleukin 20 increases in plasma and aortic tissues from patients with acute aortic dissection

Objective: Acute aortic dissection (AAD) is the most devasting cardiovascular disease associated with high mortality. The occurrence and progression of AAD can be regulated by inflammatory processes, and further understanding of this inflammatory pathogenesis may improve the treatment of AAD. Interleukin 20 (IL-20), as an inflammatory mediator, has been demonstrated to be associated with several inflammatory diseases. However, the association between IL and 20 and AAD is still unknown.

Methods: Five aortic dissection tissue samples and five control aortic tissue samples were evaluated in our study. The expression of IL-20 and its receptor subunits (IL-20Rα and IL-20Rβ) was detected by immunofluorescence staining. From January 2018 to March 2018, 70 consecutive AAD patients and 25 non-AAD (NAD) patients were enrolled in this study. Diagnosis was based on computed tomography angiography (CTA) results. Blood samples were obtained from the patients on the first day of hospitalization. Plasma IL-20, TNF-α and IL-6 concentrations were evaluated with enzyme-linked immunosorbent assay (ELISA) kits.

Results: The expression levels of IL-20 and its receptor subunits (IL-20Rα and IL-20Rβ) were increased in the sites of arterial wall dissection in the AAD patients. In a separate group, the plasma IL-20, TNF-α and IL-6 concentrations were significantly higher in the AAD patients than in the non-AAD patients. Spearman's correlation analysis showed that plasma IL-20 was positively correlated with plasma TNF-α and IL-6, D-dimer, C-reaction protein (CRP), creatinine, fasting blood glucose, systolic blood pressure (SBP), and diastolic blood pressure (DBP). Multiple linear regression revealed that IL-20, in addition to IL-6, glucose, CRP and D-dimer, was independently associated with the presence of AAD.

Conclusion: IL-20 was closely associated with the presence of AAD. IL-20 may contribute to the inflammatory pathogenesis of AAD.