Upregulation of Inflammatory Cytokines in Pulmonary Embolism Using Biochip-Array Profiling

Author:

Bontekoe Emily1ORCID,Brailovsky Yevgeniy2ORCID,Hoppensteadt Debra3ORCID,Bontekoe Jack1ORCID,Siddiqui Fakiha1ORCID,Newman Joshua4,Iqbal Omer5,Reed Trent6,Fareed Jawed3ORCID,Darki Amir7ORCID

Affiliation:

1. Department of Pathology and Laboratory Medicine, Cardiovascular Research Institute, Hemostasis and Thrombosis Research Division, Loyola University Medical Center, Health Sciences Division, Maywood, IL, USA

2. Advanced Heart Failure, Mechanical Circulatory Support, Heart Transplant, Jefferson Heart Institute, Sidney Kimmel School of Medicine, Thomas Jefferson University, Philadelphia, PA, USA

3. Department of Pathology and Laboratory Medicine and Department of Pharmacology and Neuroscience, Cardiovascular Research Institute, Hemostasis and Thrombosis Research Division, Loyola University Chicago, Health Sciences Division, Maywood, IL, USA

4. Division of Cardiovascular Medicine, Department of Medicine, Loyola University Medical Center, Maywood, IL, USA

5. Department of Pathology and Laboratory Medicine and Department of Ophthalmology, Cardiovascular Research Institute, Loyola University Medical Center, Maywood, IL, USA

6. Department of Emergency Medicine, Loyola University Medical Center, Stritch School of Medicine, Maywood, IL, USA

7. Division of Cardiology, Department of Medicine, Loyola University Medical Center, Stritch School of Medicine, Maywood, IL, USA

Abstract

The complex pathophysiology of pulmonary embolism (PE) involves hemostatic activation, inflammatory processes, cellular dysfunction, and hemodynamic derangements. Due to the heterogeneity of this disease, risk stratification and diagnosis remains challenging. Biochip-array technology provides an integrated high throughput method for analyzing blood plasma samples for the simultaneous measurement of multiple biomarkers for potential risk stratification. Using biochip-array method, this study aimed to quantify the inflammatory biomarkers such as interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, vascular endothelial growth factor (VEGF), interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and epidermal growth factor (EGF) in 109 clinically confirmed PE patients in comparison to the control group comprised of plasma samples collected from 48 healthy subjects. Cytokines IL-4, IL-6, IL-8, IL-10, IL-1β, and MCP-1 demonstrated varying level of significant increase ( P < 0.05) in massive-risk PE patients compared to submassive- and low-risk PE patients. The upregulation of inflammatory cytokines in PE patients observed in this study suggest that inflammation plays an important role in the overall pathophysiology of this disease. The application of biochip-array technology may provide a useful approach to evaluate these biomarkers to understand the pathogenesis and risk stratification of PE patients.

Publisher

SAGE Publications

Subject

Hematology,General Medicine

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