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Allergic diseases begin early in life and are often chronic, thus creating an inflammatory environment that may lead to metabolic disorders, although the underlying mechanisms remain incompletely understood. Here, we show that allergic inflammation induces diet-independent dyslipidemia in a mouse model of allergy and atherosclerosis. Using untargeted lipidomics in mouse plasma, we found that allergic inflammation induces a unique lipid signature that extends beyond acute and late inflammation and that is characterized by triglyceride (TG) changes in circulation. Alterations in blood TGs following an allergic reaction are independent of T-cell-driven late phase inflammation. On the contrary, the humoral component is sufficient to induce a TG increase and a unique lipid profile through the IgG-mediated alternative pathway of anaphylaxis. Lastly, we demonstrated blood TG changes in patients after undergoing an allergic reaction. Overall, this study reveals the importance of IgG-mediated allergic inflammation insofar as it regulates lipid metabolism, which may contribute to atherosclerosis and, ultimately, to cardiovascular events.
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bioRxiv's