Lewis Pearson
The Role Of Interleukin-1β In Coronary Artery Disease
Pearson, Lewis
Abstract
Coronary artery disease (CAD) is a leading cause of mortality worldwide, with an estimated 17.8 million CAD-associated deaths each year. A prominent pathogenic factor in CAD is inflammation, which is associated with elevated levels of the cytokine interleukin-1β (IL-1β). However, it isn’t clear to what extent IL-1β contributes to reduced cardiac function in CAD. CAD is also associated with elevations of reactive oxygen species (ROS), thus oxidative stress, though the extent to which this is dependent on elevations of IL-1β remains ambiguous. Accordingly, this preliminary study quantified IL-1β serum levels within a patient cohort using a high-sensitivity ELISA kit (Invitrogen, Massachusetts) and then correlated those levels to clinical indices of cardiac function. The effects of clinically relevant (1 pg/ml) and supraphysiological (50 ng/ml) levels of IL-1β on intracellular oxidative stress were also investigated via the use of a 2',7'-dichlorofluorescin diacetate assay. On average, IL-1β serum concentrations were 1.03 ± 0.025 pg/ml, with IL-1β levels showing a correlation with peak E- wave (n=56, p = 0.03, r2 = 0.09). In single cells, 1 pg/ml and 50 ng/ml IL-1β increased oxidative stress by 6 % (p = 0.32) and 14 % (p = 0.014), respectively. These preliminary data suggest that IL-1β does not significantly contribute to cardiac dysfunction in CAD. Furthermore, although supraphysiological concentrations of IL-1β are fundamentally capable of producing intracellular oxidative stress, clinically relevant levels are not. This suggests that IL-1β alone is not the sole cause of the increases in oxidative stress that are synonymous with CAD. As such, further investigation is required to uncover the role that IL-1β may play in the pathology of CAD.
Citation
Pearson, L. The Role Of Interleukin-1β In Coronary Artery Disease. (Thesis). University of Salford
Thesis Type | Thesis |
---|---|
Deposit Date | Nov 1, 2024 |
Award Date | Nov 21, 2024 |
This file is under embargo due to copyright reasons.
Contact l.pearson6@edu.salford.ac.uk to request a copy for personal use.
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