Cytokines at the Interplay Between Asthma and Atherosclerosis?

Abstract

Cardiovascular disease (CVD) is an important comorbidity in a number of chronic inflammatory diseases. However, evidence in highly prevalent respiratory disease such as asthma are still limited. Epidemiological and clinical data are not univocal in supporting the hypothesis that asthma and CVD are linked and the mechanisms of this relationship remain poorly defined. In this review, we explore the relationship between asthma and cardiovascular disease, with a specific focus on cytokine contribution to vascular dysfunction and atherosclerosis. This is important in the context of recent evidence linking broad inflammatory signaling to cardiovascular events. However inflammatory regulation in asthma is different to the one typically observed in atherosclerosis. We focus on the contribution of cytokine networks encompassing IL-4, IL-6, IL-9, IL-17A, IL-33 but also IFN-g and TNF-a to vascular dysfunction in atherosclerosis. In doing so we highlight areas of unmet need and possible therapeutic implications.

Shared Genetic Architecture and Causal Relationship Between Asthma and Cardiovascular Diseases: A Large-Scale Cross-Trait Analysis

“…A previous study indicates that cytokines that are up-regulated in asthma may promote the migration and activation of inflammatory cells implicated in atherogenesis ( Halasz et al, 2002 ; Zietkowski et al, 2007 ; Zietkowski et al, 2010 ), and cytokines are also important mediators of bronchoconstriction in asthma ( Hiemstra et al, 2015 ). Leukotrienes as a kind of cytokines found in asthmatic bronchioles also exhibits strong proinflammatory activities in cardiovascular tissues ( Spanbroek et al, 2003 ; Gurgone et al, 2020 ). Previous studies have shown that pyroptosis not only plays an important role in infectious diseases but is also associated with CVDs, central nervous system diseases, and tumors ( Gong et al, 2020 ; Zhou et al, 2020 ).…”

Why do some asthma patients respond poorly to glucocorticoid therapy?

“…As examples of acquired GC resistance, inflammation or oxidative stress can negatively affect GR signaling [ 22 ] Possible mechanisms for acquired resistance could be related to immune dysregulation; for example, interleukin (IL)-2, IL-4 and IL-13 are often overexpressed in the lungs of steroid insensitive patients [ [44] , [45] , [46] ]. This profile of cytokine up-regulation is associated with reduced GR affinity in vitro through activation of p38 mitogen-activated protein kinase resulting in the phosphorylation of GR and diminished nuclear translocation in inflammatory cells [ 47 ].…”

The association between serum apolipoprotein B and fractional exhaled nitric oxide in bronchial asthma patients

“…Asthma and lipid metabolism are associated with systemic inflammation. Asthma and atherosclerosis are characterized by the accumulation of immune cells, activation of mast cells and smooth muscle cells, and increased immunoglobulin E (Ig E) levels (4,5). Activation of the immune system, triggers the release of cytokines, which affects fatty acid oxidation, activating lipoprotein lipase and hepatic lipase, causing dyslipoproteinemia (6,7).…”