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Transglutaminase (TGase)-mediated crosslinking serves as a promising strategy to mitigate soy antigenicity. β-Conglycinin is recognized as a key allergen among soy proteins. Nonetheless, our understanding of the underlying relationship between immunoreactivity and protein structure remains inadequate. This study aimed to examine the impact of TGase-mediated crosslinking on the immunoreactivity of β-conglycinin in a dual-protein system consisting of soy protein isolate (SPI) and whey protein isolate (WPI) (with SPI-WPI ratios of 10:0, 7:3, 5:5, 3:7 (w/w)). Conformational changes were also examined. Results revealed that β-lactoglobulin and α-lactalbumin in WPI were less susceptible to TGase crosslinking compared to the 7S and 11S subunits in SPI. The conformation of proteins in the dual-protein system after TGase crosslinking were altered, as demonstrated by increased ultraviolet absorption intensity, fluctuant intrinsic fluorescence intensity and surface hydrophobicity, and decreased free sulfhydryl content. As the crosslinking time of TGase increased from 1 h to 18 h, the allergenicity of β-conglycinin gradually decreased in all four SPI-WPI ratios. Notably, the SPI3-WPI7 ratio exhibited the lowest allergenicity of 77.21 ± 1.89% after 18 h of TGase catalyzation. Overall, the dual-protein system proved to be more effective in reducing the allergenicity of β-conglycinin. [Display omitted] • TGase treatment can alter the conformation of soy-cow milk allergenic proteins. • Using TGase can reduce the antigenicity of β-conglycinin, especially in dual-protein system. • SPI3-WPI7 treated by TGase for 18 h had the lowest antigenicity. • TGase crosslinking may be efficient to produce hypoallergenic dual-protein products. [ABSTRACT FROM AUTHOR]

• Early-life airways infection with Streptococcus pneumonia aggravated airways hyperresponsiveness, inflammation and airway remodelling in the HDM-induced allergic asthma model. • This infection promoted expression of IL-25, IL-33, TSLP and expansion of Th2 and ILC2 cells in the lungs of HDM -induced allergic asthma model. • Our data suggest that early-life Streptococcus pneumonia airways infection may not only increase the risk of development of allergic asthma following HDM sensitisation later in life, but also increase the severity of the disease. Respiratory tract infection early in life plays a significant role in the pathogenesis of asthma. In the present study we examine, using a murine surrogate, the effects of early life respiratory infection with Streptococcus pneumoniae (SP) on adult asthma induced by sensitisation and exposure to house dust mite (HDM) allergen. Mice (one week old) were infected with SP, then 3 weeks later sensitised to HDM emulsified with Al (OH)3 intraperitoneally and challenged intranasally with same allergen for up to a further 5 weeks to establish the asthma surrogate. Outcome measures were quantified using the FlexiVent apparatus, histology and immunohistology, ELISA and flow cytometry. The murine surrogates of asthma infected with SP early in life exhibited significantly more severe disease compared with the controls of mice without SP infection, as shown by airways responsiveness, inflammatory cellular infiltration of the airways, expression of markers of airways remodelling, serum concentrations of HDM-specific IgE and the concentrations of Th2-type cytokines and the numbers of activated Th2 and ILC2 cells in the lung tissues. These data are compatible with the hypothesis that early-life infection of the airways with SP exacerbates, at least in some individuals, subsequent HDM-induced allergic airways inflammation and associated asthma in adulthood in this murine surrogate. [ABSTRACT FROM AUTHOR]