D1.287 - Lipid profiling of Co-factor Induced Anaphylaxis: The Impact of Exercise and Aspirin on metabolism

Poster abstract

Background

Food allergies, affecting approximately 13% of the population in Europe, is a significant public health concern. In southern Europe, lipid transfer protein (LTP) allergy is the most common primary food allergy, with clinical manifestations ranging from mild urticaria to severe anaphylaxis. Cofactors can enhance allergic responses or trigger anaphylaxis, with some individuals only experiencing reactions when cofactors are present. This study aims to investigate the mechanisms behind the cofactor effect in LTP anaphylaxis by assessing whether aspirin/exercise induce a distinct metabolic signature even in the absence of allergen exposure. 

Method

Four adult groups were recruited: cofactor-induced LTP anaphylaxis (A) (n=9), LTP-sensitized individuals with no food allergy (B) (n=5), atopic controls (with asthma/rhinitis but no food allergy) (C) (n=6), and healthy controls (D) (n=6). Serum samples were collected on fasting conditions on two separate days. At visit 1, patients underwent an exercise test in accordance with SEPAR guidelines (Perpiñá Tordera M, et al. Arch Bronconeumol 2013) on exercise-induced asthma. At visit 2, patients took 500 mg of aspirin. Serum samples were taken before the cofactor (T0) and at 2 points post-treatment/ intervention (30min for exercise, 1h for aspirin, and 2h for both). Lipidomic analysis of samples was performed using liquid chromatography coupled with mass spectrometry (LC-MS).

Results

Across all study groups, exercise affects a higher number of fatty acids (FA) and carnitines (CAR) compared to aspirin exposure. Additionally, serum oxylipin analysis revealed a significant increase in 12,13 DiHOME levels 2h after exercise (p=0.005) and a decrease in thromboxane levels 1h after aspirin intake (p=0.033). Comparing groups (A) and (D), we identified the following metabolic changes: for exercise, increased levels of FA, including palmitoleic, myristic, and myristoleic acid, were observed both before and after exercising, while the increase in nervonic and margaric acid appeared only post-treatment. Furthermore, 120 minutes after aspirin intake, the levels of CAR 13:1, palmitoleic and myristoleic acid were increased.

Conclusion

Patients with anaphylaxis showed differences in proinflammatory and anti-inflammatory metabolites in response to cofactor, even in the absence of the allergen, pointing towards an intrinsic underlying mechanism that needs to be further explored.