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The concentration of interleukin-33 in heart failure with reduced ejection fraction
Oliwia Anna Segiet1, Ewa Romuk2, Ewa Nowalany-Kozielska1
1Department of 2nd Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia; Katowice-Poland.
Insights
Interleukin-33 (IL-33) levels are significantly lower in heart failure (HF) patients compared to healthy individuals. Lower IL-33 concentrations are also observed in patients with ischemic heart failure and unstable disease, suggesting its role in HF progression.
Area of Science:
- Cardiology
- Immunology
Background:
- Heart failure (HF) remains an incurable, progressive condition.
- Inflammation is implicated in the initiation and progression of HF.
Purpose of the Study:
- To investigate the role of interleukin-33 (IL-33) in the pathogenesis of heart failure.
- To determine if disease etiology and disease course influence cytokine expression in HF.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure IL-33 concentrations.
- Study included 155 patients with systolic HF and 60 healthy controls.
Main Results:
- IL-33 concentrations were significantly lower in HF patients (16.91 pg/mL) than in healthy subjects (92.51 pg/mL).
- Patients with ischemic HF had lower IL-33 levels (10.75 pg/mL) than those with non-ischemic HF (21.05 pg/mL).
- Stable HF patients exhibited lower IL-33 levels (10.46 pg/mL) compared to unstable HF patients (19.02 pg/mL).
Conclusions:
- Lower IL-33 concentrations in HF patients suggest a role in disease development and progression.
- Interleukin levels vary based on the etiology and severity of heart failure.
Objective:
Despite several improvements in the management of heart failure (HF), it is still an incurable and a progressive disease. Several trials demonstrated that the process of inflammation may be responsible for initiation and progression of HF. The aim of the present study was to investigate the role of interleukin-33 (IL-33) in the pathogenesis of HF and to assess whether disease etiology and course of the disease affect the expression of cytokines.
Methods:
The study included 155 (106 male and 49 female) patients with systolic HF with a mean left ventricle ejection fraction of 32.13+-12.8% and 60 (36 male and 24 female) healthy individuals. IL-33 concentrations were evaluated using enzyme-linked immunosorbent assay.
Results:
The concentration of IL-33 was statistically significantly lower in patients with HF than in healthy subjects, 16.91 (0-81.00) pg/mL and 92.51 (33.61-439.61) pg/mL, respectively. Patients with HF with ischemic etiology had lower concentration of IL-33 (10.75 pg/mL) than subjects with HF with non-ischemic etiology (21.05 pg/mL). Patients with stable HF (10.46 pg/mL) had lower IL-33 levels than those with unstable HF (19.02 pg/mL).
Conclusion:
The concentrations of IL-33 were lower in patients with HF than in healthy controls, which may play an important role of above cytokine in HF development and progression. In addition, interleukin concentrations varied depending on the etiology and severity of the course of the disease.
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