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To enrich the flavor and nutritional efficacy of soymilk powder, this study investigated the effects of adding different ratios of pea peptides on the quality, nutrition and flavor of soymilk powder. The reconstitutability of soymilk powder was examined based on solubility and caking rate, and its in vitro bioactive functions were evaluated in terms of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and cholesterol scavenging capacity. The changes in the structural properties and flavor quality of soymilk powder caused by addition of pea peptides were explored by Fourier transform infrared (FTIR) spectroscopy, nanoparticle size analyzer, confocal laser scanning microscopy (CLSM), and headspace solid phase microextraction (HS-SPME)-gas chromatography-mass spectrometry (GC-MS). The results showed that the addition of 30% pea peptides to soymilk powder increased the protein content by 13.05% and solubility by 11.23%, decreased the caking rate by 4.20%, enhanced the DPPH radical and cholesterol scavenging capacity by 19.84% and 21.25%, respectively, and significantly improved the reconstitutability in hot water at 70 ℃. The structural analysis results revealed that pea peptide addition altered the secondary structure of proteins, reduced the average particle size, and resulted in more uniform particle size distribution in reconstituted soymilk, thereby improving the solubility of soymilk powder. Additionally, pea peptide addition changed the concentrations of the key flavor components geranylacetone, myristic acid, 3-methylthiopropanal, 2-methylpyrazine and 2,5-dimethylpyrazine in reconstituted soymilk, while decreasing the concentrations of off-flavor substances, such as hexanal, trans-2-nonenal, nonanal, n-hexanol, 1-octen-3-ol and naphthalene.

Many inflammatory skin diseases are characterized by altered epidermal differentiation. Whether this altered differentiation promotes inflammatory responses has been unknown. Here, we show that IRAK2, a member of the signaling complex downstream of IL-1 and IL-36, correlates positively with disease severity in both atopic dermatitis and psoriasis. Inhibition of epidermal IRAK2 normalizes differentiation and inflammation in two mouse models of psoriasis- and atopic dermatitis-like inflammation. Specifically, we demonstrate that IRAK2 ties together proinflammatory and differentiation-dependent responses and show that this function of IRAK2 is specific to keratinocytes and acts through the differentiation-associated transcription factor ZNF750. Taken together, our findings suggest that IRAK2 has a critical role in promoting feed-forward amplification of inflammatory responses in skin through modulation of differentiation pathways and inflammatory responses.

BackgroundAlthough multiple studies have assessed molecular changes in chronic atopic dermatitis (AD) lesions, little is known about the transition from acute to chronic disease stages, and the factors and mechanisms that shape chronic inflammatory activity.ObjectivesWe sought to assess the global transcriptome changes that characterize the progression from acute to chronic stages of AD.MethodsWe analyzed transcriptome changes in paired nonlesional skin, acute and chronic AD lesions from 11 patients and 38 healthy controls by RNA-sequencing, and conducted in vivo and histological assays to evaluate findings.ResultsOur data demonstrate that approximately 74% of the genes dysregulated in acute lesions remain or are further dysregulated in chronic lesions, whereas only 34% of the genes dysregulated in chronic lesions are altered already in the acute stage. Nonlesional AD skin exhibited enrichment of TNF, TH1, TH2, and TH17 response genes. Acute lesions showed marked dendritic-cell signatures and a prominent enrichment of TH1, TH2, and TH17 responses, along with increased IL-36 and thymic stromal lymphopoietin expression, which were further heightened in chronic lesions. In addition, genes involved in skin barrier repair, keratinocyte proliferation, wound healing, and negative regulation of T-cell activation showed a significant dysregulation in the chronic versus acute comparison. Furthermore, our data show progressive changes in vasculature and maturation of dendritic-cell subsets with chronicity, with FOXK1 acting as immune regulator.ConclusionsOur results show that the changes accompanying the transition from nonlesional to acute to chronic inflammation in AD are quantitative rather than qualitative, with chronic AD having heightened TH2, TH1, TH17, and IL36 responses and skin barrier repair mechanisms. These findings provide novel insights and highlight underappreciated pathways in AD pathogenesis that may be amenable to therapeutic targeting.