Abstract
Atherosclerosis (AS) is a major pathologic sequel of obesity. It causes cardiovascular disease (CVD), the most common contributor to death in the Western world. A systemic chronic low-grade immune-mediated inflammation (scLGI) is substantially involved in AS and CVD. Pro-inflammatory cytokines released during cellular immunity play a major role, with the Th1-type cytokine interferon-gamma (IFN-γ) being a key mediator. Among other effects, IFN-γ activates the enzyme indoleamine 2,3-dioxygenase (IDO) in monocyte-derived macrophages, dendritic, and other cells, which ultimately decreases serum levels of the essential amino acid tryptophan (TRP). Hence, patients with CVD show increased serum kynurenine to tryptophan concentrations (KYN/TRP), a result of an increased TRP degradation. Importantly, a strong increased KYN/TRP is associated with a higher likelihood of fatal cardiovascular outcomes. Moreover, an increased production of the pro-inflammatory adipokine leptin, in combination with IFN-γ and interleukin-6 (IL-6), represents a central link between obesity, AS, and CVD. Leptin has also been shown to be involved in a Th1-weighted T cell polarization.
Published Version
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