Speaker
Description
We consider a previously developed qualitative model for the inflammatory response in atherosclerosis and extend it to account for time-dependent anti-oxidant and anti-inflammatory therapies. The model consists of a five-dimensional system of ordinary differential equations tracking the concentrations of LDL, free radicals, oxidized LDL, macrophages and cytokines. Drug actions are incorporated through time-decaying efficacy factors that reduce the oxidation rate of LDL and the cytokine-mediated amplification of inflammation. We characterize the existence and uniqueness of an inflammatory equilibrium, and derive explicit conditions for its local asymptotic stability in terms of biologically interpretable parameters.
We then investigate numerically several therapeutic scenarios, including no therapy, mono-therapies and a combination therapy acting simultaneously on oxidative stress and cytokine amplification. Then we perform numerical simulations for the system. Time courses of oxidized LDL, macrophages and cytokines, as well as numerical bifurcation diagrams of the steady-state cytokine level with respect to drug intensities and to the cytokine production rate, are presented and interpreted. Our results suggest that the combination therapy yields a pronounced synergistic reduction of both oxidized LDL and inflammatory burden, and can move the system from a high-inflammatory regime to a low-inflammatory one in agreement with the qualitative stability analysis.
Bibliography
Abi Younes, G., Chahrour, Y., El Hajj, W., & El Khatib, N. (2025). A Qualitative Analysis of the Inflammatory Response in Atherosclerosis with Emphasis on LDL Oxidation. Math. Model. Nat. Phenom., 20, 19. doi:10.1051/mmnp/2025018.