Allergic asthma accelerates atherosclerosis dependent on Th2 and Th17 in apolipoprotein E deficient mice

Aims. The chronic inflammation of atherosclerosis is regulated by Th1, while allergic asthma is controlled by Th2. The direct relationship between atherosclerosis and asthma is contradictory. The aim of this study was to investigate the role of allergic asthma in atherosclerotic plaque formation and the change of CD4+ T cells subsets. Methods and results. Six-week C57BL/6J or apoE−/− mice were sensitized on day 0, 7 and 14, then exposed to aerosolized 1% Ovalbumin (OVA) or PBS 30 min/day, 3 times/week for 8 or 16 weeks from day 14 onward. The results showed that allergic asthma mice models were successfully established and the accelerated atherosclerosis induced by allergic asthma accompanied with increased Th2 and Th17 cells but not Th1 cells in spleen. Moreover, the expression and production of Th2 and Th17 biomarkers including IL-4 and IL-17A were significantly elevated in asthmatic apoE−/− mice. After 8-week treated with the neutralizing antibody of IL-4 or IL-17A, the lesion area in the aortic root of asthmatic apoE−/− mice was markedly decreased, and more dramatical result was observed after the combined treatment with IL-4 and IL-17A mAbs. The expression of IgE and FcεRIα in the aortic root of apoE−/− mice was markedly increased but was significantly reduced after 8-week treatment with IL-4 mAb. Conclusion. Allergic asthma accelerates atherosclerosis by modulating the balance of Teff/Treg cells in apoE−/− mice, which is associated with increased Th2 and Th17 cells but not Th1 cells.