B enite, d the National Referee Centre for Rheumatic and AutoImmune and Systemic diseases in childrEn (RAISE), and

Background: Peach is a common elicitor of food allergic reactions. Peach-induced immediate reactions may occur as benign pollen-food syndromes, usually due to birch pollen-related PR-10 cross-reactivity in temperate climates, and as potentially severe primary food allergies, predominantly related to nsLTP Pru p 3 in Mediterranean regions. The newly described peach allergen Pru p 7 has gained recent attention as a potential peach allergy severity marker. Sensitization to Pru p 7 and its allergenic homologues of the gibberellin-regulated protein family occurs in areas with high Cupressaceae tree pollen exposure. Objective:We sought to investigate the distribution, clinical characteristics and molecular associations of Pru p 7 sensitization among subjects with suspected peach allergy in different regions of France. Methods: Subjects with suspected peach allergy (n = 316) were included. Diagnostic work-up was performed according to current guidelines, including open food challenge when required. IgE antibody measurements and competition experiments were performed using the ImmunoCAP assay platform. Results: Sensitization to Pru p 7 was present in 171 (54%) of all subjects in the study and in 123 of 198 (62%) diagnosed as peach allergic, more than half of whom were sensitized to no other peach allergen. Frequency and magnitude of Pru p 7 sensitization were associated with the presence of peach allergy, the clinical severity of peach-induced allergic reactions and the level of cypress pollen exposure. Cypress pollen extract completely outcompeted IgE binding to Pru p 7. Pru p 7 was extremely potent in basophil activation tests. Conclusion and Clinical Relevance: A subtype of Cupressaceae pollinosis, characterized by Pru p 7 sensitization, can be an underlying cause of severe peach allergy. K E Y W O R D S allergens and epitopes, anaphylaxis, basophil, cypress pollinosis, food allergy, IgE, immunological tests, peamaclein, Pru p 7

No abstract

Scope Enhanced adiposity and metabolic inflammation are major features of obesity associated with altered gut microbiota and intestinal barrier. How these metabolic outcomes can be impacted by milk polar lipids (MPL), naturally containing 25% of sphingomyelin, is investigated in mice fed a mixed high‐fat (HF) diet . Methods and results Male C57Bl/6 mice receive a HF‐diet devoid of MPL (21% fat, mainly palm oil, in chow), or supplemented with 1.1% or 1.6% of MPL (HF‐MPL1; HF‐MPL2) via a total‐lipid extract from butterserum concentrate for 8 weeks. HF‐MPL2 mice gain less weight versus HF (p < 0.01). Diets do not impact plasma markers of inflammation but in the liver, HF‐MPL2 tends to decrease hepatic gene expression of macrophage marker F4/80 versus HF‐MPL1 (p = 0.06). Colonic crypt depth is the maximum in HF‐MPL2 (p < 0.05). In cecal microbiota, HF‐MPL1 increases Bifidobacterium animalis versus HF (p < 0.05). HF‐MPL2 decreases Lactobacillus reuteri (p < 0.05), which correlates negatively with the fecal loss of milk sphingomyelin‐specific fatty acids (p < 0.05). Conclusion In mice fed a mixed HF diet, MPL can limit HF‐induced body weight gain and modulate gut physiology and the abundance in microbiota of bacteria of metabolic interest. This supports further exploration of how residual unabsorbed lipids reaching the colon can impact HF‐induced metabolic disorders.