Bovine β-Lactoglobulin (BLG) induces severe cow’s milk allergy. This research investigated the effect of ultrasound-assisted luteolin (LUT) treatment on the structure and allergenicity of BLG. The structure of the treated BLG was characterized by Fourier transform infrared (FTIR) spectroscopy, circular dichroism (CD) spectroscopy, ultraviolet (UV) absorption spectroscopy and fluorescence spectroscopy, and its allergenicity was evaluated by enzyme-linked immunosorbent assay (ELISA) and cell experiments. It was found that the major interaction force between BLG and LUT was hydrophobic interaction both before and after ultrasonic treatment. Ultrasound-assisted LUT treatment significantly altered the secondary and tertiary structures of BLG, and reduced the IgE-binding ability and the release of interleukin-6, interleukin-4 and histamine from KU812 cells. Therefore, ultrasound-assisted LUT treatment changes the conformational epitope of BLG, reducing its allergenicity, and the best effect can be achieved by secondary ultrasound-assisted LUT treatment.

The rising incidence of food allergy attracts researchers to advocate that a high-fat diet (HFD) is an attention-grabbing trigger. However, the mechanism by which HFD aggravates food allergy remains largely unknown. In this context, intestinal epithelium dysfunction as a characteristic of food allergy is summarized. Specifically, we focus our attention on the microbiota-intestinal epithelium interactions and call attention to the underlying mechanism by which HFD promotes food allergy along the interactions. Escaped fat and excessed bile acids in the colon induced by HFD can disrupt gut microbiota, directly regulating intestinal epithelium function. Additionally, HFD contributes to indirectly destroying the intestinal epithelium and enhancing its permeability by altering the level of microbial metabolites. Consequently, these ways promote the influx of food allergens. Substantial quantities of food allergens traverse the intestinal epithelium, prompting heightened secretion of pro-inflammatory cytokines, thus favoring a Th2 immune response. In this situation, impaired differentiation of Treg and Th1 cells can aggravate food allergy. Clarifying the intricate relationship between HFD and food allergy from the microbiota-intestinal epithelium interactions may offer prevention strategies for food allergy.