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Upregulation of Inflammatory Biomarkers in Pulmonary Embolism as Studied by a Biochip- Array Profiling Approach

E. Bontekoe, E. Brailovsky, D. Hoppensteadt, F. Siddiqui, A. Farooqui, O. Iqbal, M. Latz, J. Fareed, A. Darki

Loyola University Medical Center, Maywood, United States

Abstract Number: PB0442

Meeting: ISTH 2020 Congress

Theme: Diagnostics and OMICs » Biomarkers of Thrombosis and Hemostasis

Background: The pathophysiology of pulmonary embolism (PE) is complex including both the systemic and localized involvement. Hemostatic activation, inflammatory processes, and cellular dysfunction, along with hemodynamic aberrations contribute to the progression and outcome of PE. Inflammatory mediators such as the interleukins, oxidative stress molecules, and other cellular products contribute to the overall pathophysiology.

Aims: The purpose of this study is to profile biomarkers of inflammatory processes in the baseline blood samples collected from patients diagnosed with PE.

Methods: Citrated blood plasma samples from patients with clinically confirmed diagnosis (n=119) were collected under an IRB approved protocol. These samples were retrospectively analyzed for such biomarkers as IL2, IL4, IL6, IL8, IL10, vascular endothelial growth factor (VEGF), gamma interferon (IFNG), tumor necrosis factor a (TNFa), IL1a, IL1b, monocyte chemotactic protein (MCP1), and epidermal growth factor (EGF). The Randox Signature System (Crumlin, North Ireland, UK) was used for profiling these markers. The control samples represented a pool prepared from healthy normal individuals for the comparison of each of these biomarkers.

Results: In comparison to the normal controls, marked increase in IL6 (53 fold), IL8 (8 fold), IL10 (6 fold), VEGF (0.9 fold), TNFa (0.9 fold), IL1a (0.5 fold), IL1b (0.7 fold), MCP1 (0.5 fold), EGF (4 fold). In contrast, IL2 (14%), IL4 (3%), and IFNG (25%) showed a decrease in the circulating levels in PE patients in comparison to the controls. Marked variations in the circulating levels of such biomarkers as IL6, IL8, IL 10 and VEGF were evident by a large scatter in the data. No correlation between the individual mediators profiled in this study was noted.

Conclusions: These results demonstrate that the pathophysiology of PE is associated with the activation of inflammatory processes resulting in the upregulation of various biomarkers. IL6, IL8, and IL10 showed the most significant increase suggesting the role of inflammation in PE.

To cite this abstract in AMA style:

Bontekoe E, Brailovsky E, Hoppensteadt D, Siddiqui F, Farooqui A, Iqbal O, Latz M, Fareed J, Darki A. Upregulation of Inflammatory Biomarkers in Pulmonary Embolism as Studied by a Biochip- Array Profiling Approach [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/upregulation-of-inflammatory-biomarkers-in-pulmonary-embolism-as-studied-by-a-biochip-array-profiling-approach/. Accessed October 2, 2023.

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